Patterns of Holocene relative sea level change in the North of Britain and Ireland

Temporal and spatial patterns of relative sea level (RSL) change in the North of Britain and Ireland during the Holocene are examined. Four episodes, each defined by marked changes in the RSL trend, are identified. Each episode is marked by a rise to a culminating shoreline followed by a fall. Episode HRSL-1 dates from the Younger Dryas to early in the Holocene; HRSL-2 to HRSL-4 occurred later in the Holocene. There is extensive evidence for each episode, and on this basis the spatial distribution of the altitude data for three culminating shorelines and a shoreline formed at the time of the Holocene Storegga Slide tsunami (ca 8110 ± 100 cal. BP) is analysed. Ordinary Kriging is used to determine the general pattern, following which Gaussian Trend Surface Analysis is employed. Recognising that empirical measurements of RSL change can be unevenly distributed spatially, a new approach is introduced which enables the developing pattern to be identified. The patterns for the most widely occurring shorelines were analysed and found to be similar and common centre and axis models were developed for all shorelines. The analyses described provide models of the spatial pattern of Holocene RSL change in the area between ca 8100 cal. BP and ca 1000 cal. BP based on 2262 high resolution shoreline altitude measurements. These models fit the data closely, no shoreline altitude measurement lying more than −1.70 m or +1.82 m from the predicted value. The models disclose a similar pattern to a recently published Glacial Isostatic Adjustment model for present RSL change across the area, indicating that the overall spatial pattern of RSL change may not have varied greatly during the last ca 8000 years.

Determining the Sun's influence on Lateglacial and Holocene climates: a focus on climate response to centennial-scale solar forcing at 2800 cal. BP

The influence of solar variability on the climate of the Lateglacial and Holocene periods has been the subject of increasing discussion during the last decade. In the Mid-Holocene, several studies have identified cold/wet events that occur at ca 2800 cal. BP and a link with a reduction in solar activity, inferred from the C-14 record, has been postulated. We present results from a multi-proxy study of peat humification, plant macrofossils and testate amoebae from a raised bog at Glen West, northwest Ireland, that indicate that dry bog surface conditions were experienced in the north of Ireland at the time of the solar anomaly starting at 2800 cal. BP. With the aid of C-14 wiggle-matching and tephrochronology, an abrupt shift to wetter conditions is dated to ca 2700 cal. BP, coinciding with a C-14 maximum but clearly post-dating the 2800 cal. BP event identified elsewhere in Europe. We explore the significance of this apparent lag in the Irish record, considering the possible role of the ocean in generating spatial and temporal complexities in the climate patterns of the North Atlantic region. We conclude that these complexities are likely to give rise to time-transgressive climate responses around the North Atlantic that will only be recognised by more critical chronological approaches.

Carbachol triggers RyR-dependent Ca(2+) release via activation of IP(3) receptors in isolated rat gastric myocytes.

Possible interactions between different intracellular Ca(2+) release channels were studied in isolated rat gastric myocytes using agonist-evoked Ca(2+) signals. Spontaneous, local Ca(2+) transients were observed in fluo-4-loaded cells with linescan confocal imaging. These were blocked by ryanodine (100 microM) but not by the inositol 1,4,5-trisphosphate receptor (IP(3)R) blocker, 2-aminoethoxydiphenyl borate (100 microM), identifying them as Ca(2+) sparks. Caffeine (10 mM) and carbachol (10 microM) initiated Ca(2+) release at sites which co-localized with each other and with any Ca(2+) spark sites. In fura-2-loaded cells extracellular 2-aminoethoxydiphenyl borate and intracellular heparin (5 mg ml(-1)) both inhibited the global cytoplasmic [Ca(2+)] transient evoked by carbachol, confirming that it was IP(3)R-dependent. 2-Aminoethoxydiphenyl borate and heparin also increased the response to caffeine. This probably reflected an increased Ca(2+) store content since 2-aminoethoxydiphenyl borate more than doubled the amplitude of transients evoked by ionomycin. Ryanodine completely abolished carbachol and caffeine responses but only reduced ionomycin transients by 30 %, suggesting that blockade of carbachol transients by ryanodine was not simply due to store depletion. Double labelling of IP(3)Rs and RyRs demonstrated extensive overlap in their distribution. These results suggest that carbachol stimulates Ca(2+) release through co-operation between IP(3)Rs and RyRs, and implicate IP(3)Rs in the regulation of Ca(2+) store content.

Extreme ultraviolet emission lines of Ca XV in solar and laboratory spectra

New R-matrix calculations of electron impact excitation rates in Ca XV are used to derive theoretical electron density diagnostic emission line intensity ratios involving 2s(2)2p(2)- 2s2p(3) transitions, specifically R-1 = I(208.70 Angstrom)/I(200.98 Angstrom), R-2 = I(181.91 Angstrom)/I(200.98 Angstrom), and R-3 = I(215.38 Angstrom)/I(200.98 Angstrom), for a range of electron temperatures (T-e = 10(6.4)-10(6.8) K) and densities (Ne = 10(9)-10(13) cm(-3)) appropriate to solar coronal plasmas. Electron densities deduced from the observed values of R-1, R-2, and R-3 for several solar flares, measured from spectra obtained with the Naval Research Laboratory's S082A spectrograph on board Skylab, are found to be consistent. In addition, the derived electron densities are in excellent agreement with those determined from line ratios in Ca XVI, which is formed at a similar electron temperature to Ca XV. These results provide some experimental verification for the accuracy of the line ratio calculations, and hence the atomic data on which they are based. A set of eight theoretical Ca XV line ratios involving 2s(2)2p(2)-2s2p(3) transitions in the wavelength range similar to140-216 Angstrom are also found to be in good agreement with those measured from spectra of the TEXT tokamak plasma, for which the electron temperature and density have been independently determined. This provides additional support for the accuracy of the theoretical line ratios and atomic data.

Preproendothelin-1 expression in human mesangial cells: evidence for a p38 mitogen-activated protein kinase/protein kinases- C-dependent mechanism

Endothelin-1 (ET-1) has been implicated in the pathogenesis of renal inflammation. This study investigated the mechanisms underlying the synergistic upregulation of preproET-1 gene expression in human mesangial cells after co-stimulation with thrombin and tumor necrosis factor alpha (TNFalpha). Whereas thrombin induced a moderate upregulation of preproET-1 mRNA, co-stimulation with TNFalpha resulted in a strong and protracted upregulation of this mRNA species. Thrombin+TNFalpha-induced upregulation of preproET-1 expression was found to require p38 mitogen-activated protein kinase and protein kinases C, whereas activation of extracellular signal-regulated kinase, c-Jun-N-terminal kinase, or intracellular Ca(2+) release were not required. Actinomycin D chase experiments suggested that enhanced stability of preproET-1 mRNA did not account for the increase in transcript levels. PreproET-1 promoter analysis demonstrated that the 5'-flanking region of preproET-1 encompassed positive regulatory elements engaged by thrombin. Negative modulation of thrombin-induced activation exerted by the distal 5' portion of preproET-1 promoter (-4.4 kbp to 204 bp) was overcome by co-stimulation with TNFalpha, providing a possible mechanism underlying the synergistic upregulation of preproET-1 expression by these two agonists. In conclusion, human mesangial cell expression of preproET-1 may be increased potently in the presence of two common proinflammatory mediators, thereby providing a potential mechanism for ET-1 production in inflammatory renal disease.

Marine04 marine radiocarbon age calibration, 0-26 cal kyr BP

New radiocarbon calibration curves, IntCal04 and Marine04, have been constructed and internationally ratified to replace the terrestrial and marine components of IntCal98. The new calibration data sets extend an additional 2000 yr, from 0–26 cal kyr BP (Before Present, 0 cal BP = AD 1950), and provide much higher resolution, greater precision, and more detailed structure than IntCal98. For the Marine04 curve, dendrochronologically-dated tree-ring samples, converted with a box diffusion model to marine mixed-layer ages, cover the period from 0–10.5 cal kyr BP. Beyond 10.5 cal kyr BP, high-resolution marine data become available from foraminifera in varved sediments and U/Th-dated corals. The marine records are corrected with site-specific 14C reservoir age information to provide a single global marine mixed-layer calibration from 10.5–26.0 cal kyr BP. A substantial enhancement relative to IntCal98 is the introduction of a random walk model, which takes into account the uncertainty in both the calendar age and the 14C age to calculate the underlying calibration curve (Buck and Blackwell, this issue). The marine data sets and calibration curve for marine samples from the surface mixed layer (Marine04) are discussed here. The tree-ring data sets, sources of uncertainty, and regional offsets are presented in detail in a companion paper by Reimer et al. (this issue).

ShCal04 Southern Hemisphere Calibration, 0–11.0 Cal Kyr BP

Recent measurements on dendrochronologically-dated wood from the Southern Hemisphere have shown that there are differences between the structural form of the radiocarbon calibration curves from each hemisphere. Thus, it is desirable, when possible, to use calibration data obtained from secure dendrochronologically-dated wood from the corresponding hemisphere. In this paper, we outline the recent work and point the reader to the internationally recommended data set that should be used for future calibration of Southern Hemisphere 14C dates.

Prograded Holocene beach-ridges with superimposed dunes in north-east Ireland: mechanisms and timescales of fine and coarse beach sediment decoupling and deposition

Two depositional models to account for Holocene gravel-dominated beach ridges covered by dunes, occurring on the northern coast of Ireland, are considered in the light of infrared-stimulated luminescence ages of sand units within beach ridges, and 14C ages from organic horizons in dunes. A new chronostratigraphy obtained from prograded beach ridges with covering dunes at Murlough, north-east Ireland, supports a model of mesoscale alternating sediment decoupling (ASD) on the upper beach, rather than macroscale sequential sediment sourcing to account for prograded beach ridges and covering dunes. The ASD model specifies storm or fair-weather sand beach ridges forming at high-tide positions (on an annual basis at minimum), which acted as deflationary sources for landward foredune development. Only a limited number of such late-Holocene beach ridges survive in the observed prograded series. Beach ridges only survive when capped by storm-generated gravel beaches that are deposited on a mesoscale time spacing of 50–130 years. The morphodynamic shift from a dissipative beach face for dune formation to a reflective beach face for gravel capping appears to be controlled by the beach sand volume falling to a level where reflective conditions can prevail. Sediment volume entering the beach is thought to have fluctuated as a function of a forced regression associated with the falling sea level from the mid-Holocene highstand (ca. 6000 cal. yr BP) identified in north-east Ireland. The prograded beach ridges dated at ca. 3000 to 2000 cal. yr BP indicate that the Holocene highstand’s regressive phase may have lasted longer than previously specified.

Ca(2+)-activated Cl(-) current in sheep lymphatic smooth muscle.

Freshly dispersed sheep mesenteric lymphatic smooth muscle cells were studied at 37 degrees C using the perforated patch-clamp technique with Cs(+)- and K(+)-filled pipettes. Depolarizing steps evoked currents that consisted of L-type Ca(2+) [I(Ca(L))] current and a slowly developing current. The slow current reversed at 1 +/- 1.5 mV with symmetrical Cl(-) concentrations compared with 23.2 +/- 1.2 mV (n = 5) and -34.3 +/- 3.5 mV (n = 4) when external Cl(-) was substituted with either glutamate (86 mM) or I(-) (125 mM). Nifedipine (1 microM) blocked and BAY K 8644 enhanced I(Ca(L)), the slow-developing sustained current, and the tail current. The Cl(-) channel blocker anthracene-9-carboxylic acid (9-AC) reduced only the slowly developing inward and tail currents. Application of caffeine (10 mM) to voltage-clamped cells evoked currents that reversed close to the Cl(-) equilibrium potential and were sensitive to 9-AC. Small spontaneous transient depolarizations and larger action potentials were observed in current clamp, and these were blocked by 9-AC. Evoked action potentials were triphasic and had a prominent plateau phase that was selectively blocked by 9-AC. Similarly, fluid output was reduced by 9-AC in doubly cannulated segments of spontaneously pumping sheep lymphatics, suggesting that the Ca(2+)-activated Cl(-) current plays an important role in the electrical activity underlying spontaneous activity in this tissue. PMID: 11029279 [PubMed - indexed for MEDLINE]

Ca2+ current and Ca(2+)-activated chloride current in isolated smooth muscle cells of the sheep urethra.

1. Isolated sheep urethral cells were studied using the perforated patch clamp technique (T = 37 degrees C). Depolarizing steps ranging from -40 to -10 mV evoked an inward current that peaked within 10 ms and a slower inward current. Stepping back to the holding potential of -80 mV evoked large inward tail currents. All three currents were abolished by nifedipine (1 microM). Substitution of external Ca2+ with Ba2+ resulted in potentiation of the fast inward current and blockade of the slow current and tails. 2. Changing the chloride equilibrium potential (ECl) from 0 to +27 mV shifted the reversal potential of the tail currents from 1 +/- 1 to 27 +/- 1 mV (number of cells, n = 5). Chloride channel blockers, niflumic acid (10 microM) and anthracene-9-carboxylic acid (9AC, 1 mM), reduced the slow current and tails suggesting that these were Ca(2+)-activated Cl- currents, ICl(Ca). 4. Caffeine (10 mM) induced currents that reversed at ECl and were blocked by niflumic acid (10 microM). 5. In current clamp mode, some cells developed spontaneous transient depolarizations (STDs) and action potentials. Short exposure to nifedipine blocked the action potentials and unmasked STDs. In contrast, 9AC and niflumic acid reduced the amplitude of the STDs and blocked the action potentials. 6. In conclusion, these cells have both L-type ICa and ICl(Ca). The former appears to be responsible for the upstroke of the action potential, while the latter may act as a pacemaker current.