Elevated CA-125 and ascites: not always malignancy

Abstract
BACKGROUND: We present two clinical cases from a single institution where a final diagnosis of cardiac failure was made following the initial finding of ascites and an elevated CA 125 level. In both cases gynaecological malignancy was initially suspected.

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]

The large- and small-scale Ca IIK structure of the Milky Way from observations of Galactic and Magellanic sightlines

Aims. The large and small-scale (pc) structure of the Galactic interstellar medium can be investigated by utilising spectra of early-type stellar probes of known distances in the same region of the sky. This paper determines the variation in line strength of Ca ii at 3933.661 Å as a function of probe separation for a large sample of stars, including a number of sightlines in the Magellanic Clouds. 

Methods. FLAMES-GIRAFFE data taken with the Very Large Telescope towards early-type stars in 3 Galactic and 4 Magellanic open clusters in Ca ii are used to obtain the velocity, equivalent width, column density, and line width of interstellar Galactic calcium for a total of 657 stars, of which 443 are Magellanic Cloud sightlines. In each cluster there are between 43 and 111 stars observed. Additionally, FEROS and UVES Ca ii K and Na i D spectra of 21 Galactic and 154 Magellanic early-type stars are presented and combined with data from the literature to study the calcium column density - parallax relationship. 

Results. For the four Magellanic clusters studied with FLAMES, the strength of the Galactic interstellar Ca ii K equivalent width on transverse scales from ∼0.05-9 pc is found to vary by factors of ∼1.8-3.0, corresponding to column density variations of ∼0.3-0.5 dex in the optically-thin approximation. Using FLAMES, FEROS, and UVES archive spectra, the minimum and maximum reduced equivalent widths for Milky Way gas are found to lie in the range ∼35-125 mÅ and ∼30-160 mÅ for Ca ii K and Na i D, respectively. The range is consistent with a previously published simple model of the interstellar medium consisting of spherical cloudlets of filling factor ∼0.3, although other geometries are not ruled out. Finally, the derived functional form for parallax (π) and Ca ii column density (N_CaII) is found to be π(mas) = 1 / (2.39 × 10^-13 × N_CaII (cm^-2) + 0.11). Our derived parallax is ∼25 per cent lower than predicted by Megier et al. (2009, A&A, 507, 833) at a distance of ∼100 pc and ∼15 percent lower at a distance of ∼200 pc, reflecting inhomogeneity in the Ca ii distribution in the different sightlines studied.

Ca2+- and volume-sensitive chloride currents are differentially regulated by agonists and store-operated Ca2+ entry.

Using patch-clamp and calcium imaging techniques, we characterized the effects of ATP and histamine on human keratinocytes. In the HaCaT cell line, both receptor agonists induced a transient elevation of [Ca2+]i in a Ca2+-free medium followed by a secondary [Ca2+]i rise upon Ca2+ readmission due to store-operated calcium entry (SOCE). In voltage-clamped cells, agonists activated two kinetically distinct currents, which showed differing voltage dependences and were identified as Ca2+-activated (ICl(Ca)) and volume-regulated (ICl, swell) chloride currents. NPPB and DIDS more efficiently inhibited ICl(Ca) and ICl, swell, respectively. Cell swelling caused by hypotonic solution invariably activated ICl, swell while regulatory volume decrease occurred in intact cells, as was found in flow cytometry experiments. The PLC inhibitor U-73122 blocked both agonist- and cell swelling–induced ICl, swell, while its inactive analogue U-73343 had no effect. ICl(Ca) could be activated by cytoplasmic calcium increase due to thapsigargin (TG)-induced SOCE as well as by buffering [Ca2+]i in the pipette solution at 500 nM. In contrast, ICl, swell could be directly activated by 1-oleoyl-2-acetyl-sn-glycerol (OAG), a cell-permeable DAG analogue, but neither by InsP3 infusion nor by the cytoplasmic calcium increase. PKC also had no role in its regulation. Agonists, OAG, and cell swelling induced ICl, swell in a nonadditive manner, suggesting their convergence on a common pathway. ICl, swell and ICl(Ca) showed only a limited overlap (i.e., simultaneous activation), although various maneuvers were able to induce these currents sequentially in the same cell. TG-induced SOCE strongly potentiated ICl(Ca), but abolished ICl, swell, thereby providing a clue for this paradox. Thus, we have established for the first time using a keratinocyte model that ICl, swell can be physiologically activated under isotonic conditions by receptors coupled to the phosphoinositide pathway. These results also suggest a novel function for SOCE, which can operate as a "selection" switch between closely localized channels.

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.

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.

Excitation rates for transitions in Ca XV

Collision strengths for transitions among the energetically lowest 46 fine-structure levels belonging to the (1s(2)) 2s(2)2p(2), 2s2p(3), 2p(4), and 2s(2)2p3l configurations of Ca XV are computed, over a wide electron energy range below 300 Ryd, using the Dirac Atomic R-matrix Code (DARC) of Norrington & Grant (2003). Resonances in the threshold region have been resolved in a fine energy mesh, and excitation rates are determined over a wide electron temperature range below 10(7) K. The results are compared with those available in the literature, and the accuracy of the data is assessed.