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Flyweight Marlen Esparza told everyone around her that she'd step out of the ring after this summer's London Olympics. It seemed logical. The 23-year-old Houston-based boxer wanted to finish her college education -- she has about two years' worth of credits -- and business and entertainment opportunities were stacking up on her desk.
The inaugural women's Olympic boxing competition was an enormous success, but Esparza fell short of her own gold medal goal, bringing home a bronze instead, and found herself at loose ends when she returned. Her emotions began to shift within a week. Earlier this month, she Tweeted simply, "I'm going to 2016!!!"
Esparza is taking a few months off to rest and strategize about how she'll structure the next four years. She and trainer Rudy Silva have parted ways amicably and she's in the market for a new mentor. "I'm open to a lot of things,'' she said. "I'm not ever going to leave Texas forever, but if I have to do that to get to the Games, then yeah, I mean I'll do it. Wherever I find a good trainer that I'm comfortable with is wherever I'll be. I'm going to keep trying things out, obsessively, until I find something I'm good and comfortable with.''
Esparza spoke with ESPN.com's Bonnie D. Ford this week. These are excerpts from their conversation.
Ford: How soon after London did you reconsider your decision to retire?
Esparza: Probably the week I got back. When I make up my mind about something, I kind of don't hear what anybody says or thinks. I know what I want and that's what I'm gonna do. So I was being stubborn with myself. I had this game plan, since I can remember: Go to the Games. Win the Games. Go to school. Then I got home and I was still in that phase of thinking about what had happened and I [was] really mad about it -- but hey, I got a bronze medal, there's nothing wrong with that. To qualify to get there was the most difficult thing ever. Reality was starting to set in, what exactly happened and how it happened, but more in a positive way. And I realized, I can't stop doing this. It's really who I am. They say you're not what you do, what you do isn't who you are. But what I do is who I am and it taught me everything about myself in life, and I'm kind of lost without it. On top of that, I didn't get a gold medal. I'm still really young, I'm really healthy and I've been blessed with a lot of opportunities and a lot of doors have opened for me.
Q: So it sounds like it wasn't a light-bulb moment, it was kind of a process over a few weeks?
A: That's really how I operate. I'm not a spontaneous, make-a-decision kind of person. It definitely took a long time for me to register and admit to myself that my game plan was the wrong game plan. I don't feel complete yet -- I'll know the day when I feel complete, when I'm done, and it's not now.
Q: Did the fact that women's boxing was so well received in London play into your decision?
A: We didn't know how they were going to respond. We were just kind of worried about them not letting us into the next Games. So once everybody did love it -- I mean, the girls' tickets sold out quicker than the guys -- [the International Olympic Committee] told us there'll probably be more weight classes [in 2016], so now I know I'm not going to be getting ready for something that I don't know is going to happen.
Q: The dilemma for you is that you don't want to keep putting the rest of your life on hold to box, so what's your current thinking about how you're going to balance and juggle that with other things?
A: I had to juggle a lot when I was really, really young. As soon as I graduated from high school, I had to figure out what I was going to do about school, I had to figure out how I was going to work, because my dad was overwhelmed financially with what I was doing. I mean, my dad would pawn stuff to get me to tournaments. I had to figure out how to box, how to find a strength trainer, how to find a swimming coach. I had to figure out how to pay for it because financially I wasn't stable. Now, it's the opposite. I have all the opportunities, so the problem is how to coordinate it the right way. I'm not going to set myself up for failure. My support system went from three to 15 or something. It's going to make things a lot easier. Everybody is behind me. They know that everybody's getting something out of the fact that I'm a boxer and that's what I do. That always comes first. Every agency, every sponsorship knows that and everybody's on board.
Q: Are you still planning to go back to school?
A: I start in January. I'm going to start slowly because I know if I try to put on too much it'll be impossible. I'll never ruin my grades. I'm going to start at [the University of Houston] and [Houston Community College] -- they both said they'll help me and work with my schedule, they know the situation. I'm going to major in biology. My plan is to get my bachelors [degree] finished before 2014, and then that way when I start getting ready for the Olympics, which is a good two years of constant, hard-core, don't-see-anybody, don't-do-anything sheltered life, all I have to worry about is all the extra stuff, not school. Once I get out of the Games I'll go pre-med.
Q: What would you expect your next competition to be?
A: When's my next fight? I don't want to tell anybody I'm not going to let anybody prepare for it.
Q: Do you expect the field to be a lot deeper and stronger in Rio?
A: I think so. I hope so. Do I want to win? Yes but the long-term thing to me is -- when I'm, like, 60 years old I want to be able to watch professional women as the main event with crowds of people. Kind of like women's soccer. Now women's soccer is totally legit and better to watch sometimes than the guys. I want that to be the same thing with boxing. I think we put up with a lot, us female boxers. We stood in the shadows way too long. I'd like to make that happen and if that's what happens, people are gonna get better and that's what I want. It's going to be more difficult and challenging for me, of course, but that's just the way it is and that's the direction I want it to go.
Q: It doesn't sound like turning pro is in your long-term plan.
A: Professional is not really my style. People laugh when I say that because of all the endorsements and commercials and stuff I have, and the agencies that I work with, but I'm really not the flashy kind of -- "Let's talk about how I'm gonna beat you, I'm better than you" -- I keep those things in my head. I don't like to express those things out loud. I'm really tactile and agile which is more for amateur boxing. Let me get in, let me do what I'm supposed to do, let the better person win, shake hands, get out and go on to the next one. That's really my thing.


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To define developmental changes in atrial natriuretic peptide (ANP) secretion and in the cross talk between C-type natriuretic peptide (CNP) and ANP, we performed experiments in isolated perfused nonbeating cardiac atria isolated from rabbits between 1 and 8 wk of age. Changes in atrial pressure resulted in increases in atrial volume that rose with age and reached the peak value at 4 wk. A rise in volume change increased ANP secretion with concomitant translocation of extracellular fluid (ECF) into the atrial lumen, which increased with age and reached the peak value at 4 wk. The positive relationship between stretch-induced ANP secretion and ECF translocation shifted upward and leftward with age. CNP suppressed stretch-induced ANP secretion in the 8-wk-old group but not in the 2- and 4-wk-old groups without differences in ECF translocation and atrial volume. Therefore, the ANP secretion in terms of ECF translocation was markedly suppressed by CNP in the 8-wk-old group but not in the 2- and 4-wk-old groups. The production of cGMP by CNP in atrial tissue membranes was markedly attenuated in young rabbits. However, 8-bromo-cGMP suppressed stretch-induced ANP secretion in 2- and 8-wk-old groups. Natriuretic peptide receptor-B mRNA was similar in both groups. Therefore, we conclude that the inhibitory effect of CNP on atrial ANP secretion is developmentally regulated, being absent during normal cardiac development in young animals and intact in adult animals.
- guanylyl cyclase-B
- development
- extracellular fluid translocation
- stretch
atrial natriuretic peptide (ANP), synthesized and stored in atrial myocytes (9), is secreted into the blood stream in response to atrial distension (7, 10, 26) and causes diuresis, natriuresis, and vasodilation (9). The primary site of ANP synthesis is cardiac atria, although extracardiac tissues also produce ANP (14, 16, 21, 30). Expression of ANP mRNA is developmentally regulated in the mammalian heart (2, 3, 8, 19,30, 34, 39). ANP mRNA is expressed in both fetal cardiac atria and ventricles. Atrial ANP mRNA gradually increases with age, whereas ventricular ANP mRNA abruptly decreases (30, 39) after birth. Species differences have been reported (19, 27, 38) in the rate of appearance of atrial ANP mRNA and in the rate of decline of ventricular ANP mRNA during development. Ventricular ANP mRNA is reactivated by cardiac hypertrophy induced by volume overload or chronic hypoxia (12, 27, 30, 35). It is reported that endogenous ANP suppresses the development of cardiac myocyte hypertrophy (17), and cardiac hypertrophy is observed in transgenic mice lacking natriuretic peptide receptor-A (NPR-A) (32). Recent studies (24) strongly suggest that ANP has an antihypertrophic effect. If ANP is an important inhibitor of cardiac hypertrophy, its expression may be developmentally regulated to allow normal cardiac growth early in life.
The natriuretic peptide family is composed of ANP, brain natriuretic peptide (BNP) (36), and C-type natriuretic peptide (CNP) (37). ANP and BNP primarily originate from the heart and activate NPR-A (11). CNP, a third member of the natriuretic peptide family, is found principally in the central nervous system and vascular endothelial cells and activates NPR-B (25). CNP is known as a local regulator (13,33) rather than a general hormone because of its low plasma level, wider distribution, and diverse biological actions. In the heart, especially, paracrine/autocrine function of CNP has been reported (1, 4). CNP inhibits proliferation of cardiac fibroblasts (4) and has positive chronotropic and inotropic effects (1). Recently, we (28) have shown negative regulation of ANP secretion by CNP through the NPR-B-cGMP pathway, which markedly attenuated in hypertrophied cardiac atria (22). Therefore, we hypothesized that the negative regulation of ANP secretion by CNP may be related to developmental cardiac hypertrophy. To define developmental changes in ANP secretion and the intracardiac effect of CNP, we investigated the increasing effect of aging and the inhibitory effect of CNP on ANP secretion, using isolated perfused nonbeating atria from rabbits of different ages.
New Zealand White rabbits, aged 1, 2, 3, 4, or 8 wk, were used. All animal experimentation described in this study was conducted in accordance with the guidelines of the American Association for Accreditation of Laboratory Animal Care.
Isolated perfused atrial preparation.
An isolated perfused atrial preparation was made as previously described (7, 20). After anesthesia with thiopental sodium (20 mg/kg), a Tygon catheter was inserted into the left atrium and secured with ligatures. The cannulated atrium was transferred, fitted into an organ chamber containing buffer solution (36.5°C), and fixed with a watertight silicone rubber cap. The atrium was immediately perfused with oxygenated HEPES buffer solution at a rate of 0.1–1.0 ml/min with peristaltic pump. The buffer solution composition was (in mM) 118 NaCl, 4.7 KCl, 2.5 CaCl2, 1.2 MgSO4, 25 NaHCO3, 10 HEPES, and 10 glucose and 0.1% BSA. The pericardial buffer solution, which contained [3H]inulin to measure the translocation of extracellular fluid (ECF), was also oxygenated by silicone tubing coils located inside the organ chamber (6). Gas pressure and pH in perfusate were monitored via periodic sampling and measured with a Corning 175 automatic pH-blood gas system (Po 2 = 486.4 ± 20.7 mmHg, pH = 7.40 ± 0.08; Corning Medical and Scientific, Medfield, MA). The pericardial space of the organ chamber was sealed and connected with a calibrated microcapillary tube, through which changes in atrial volume were monitored. After stabilization for 30 min, the perfusate was collected in 2-min intervals (4-min interval in the case of 1-wk-old rabbits because of low flow rate) at 4°C. Atrial distension was induced for 2 min (4 min in the case of 1-wk-old rabbits) by elevating the position of the out-flow catheter tip to 2 cmH2O, and atrial contraction was induced by lowering the position of the catheter tip to basal level. Changes in atrial volume in terms of atrial distension followed by reduction (distension and reduction volume, DRV) were measured by changes in water column through a calibrated microcapillary tube. Atrial pressure was subsequently increased from 0 to 1, 2, 4, or 6 cmH2O for 2 min (4 min in the case of 1-wk-old rabbits) every 8 min.
RIA of ANP.
The concentration of immunoreactive ANP in atrial perfusates and tissue homogenates was measured using specific RIA as described previously (6, 7). For RIA, 50 or 100 μl of atrial perfusates were directly used. In terms of different concentrations of atrial ANP, tissue homogenates were diluted by 10 to 500-fold and 50 μl was used for the RIA. RIA was performed in Tris-acetate buffer (0.1 M, pH 7.4) containing neomycin (0.2%), EDTA (1 mM), soybean trypsin inhibitor (50Nα-benzoyl-l-arginine ethyl ester U/ml), aprotinin (200 kallikrein inhibitory units/ml), phenylmethylsulfonyl fluoride (0.4 mg%), sodium azide (0.02%), and BSA (1%). Standard and samples were incubated with anti-ANP antibody and125I-labeled ANP for 24 h at 4°C. The bound form was separated from the free form using charcoal suspension. RIA for ANP was done on the day of the experiments, and all samples in an experiment were analyzed in a single assay. The secreted amount of ANP was expressed as nanograms of ANP per minute per gram of tissue wet weight.
The molar concentration of ANP release was calculated as follows (5, 6) The denominator 3,063 refers to the molecular mass for ANP-(1–28) (in Da), since the ANP secreted was found to be mainly the processed ANP (6).
Measurement of ECF translocation.
The ECF translocated from the atria was measured as described previously (5, 6). Radioactivity in perfusate and pericardial buffer solution was measured with a liquid scintillation counter, and the amount of ECF translocated through atrial wall was calculated as follows
Activation of particulate guanylyl cyclase in atrial membranes.
Particulate guanylyl cyclase (GC) activity was measured by determination of cGMP generated in protein aliquots of atrial tissue membranes, as described previously (23). Briefly, left atrial tissues obtained from rabbits of different ages were homogenized at 4°C in 30 mM phosphate buffer (pH 7.2) containing 120 mM NaCl and 1 mM phenanthroline by three 30-s bursts of 27,000 rpm. The homogenates were centrifuged at 1,500 g for 10 min at 4°C, and the supernatants were recentrifuged at 40,000 g for 60 min at 4°C. The membrane pellets were washed three times with 50 mM Tris · HCl (pH 7.4) and resuspended in this solution. Protein contents were determined using a bicinchoninic acid assay kit. Particulate GC activity was measured in protein aliquots of tissue membranes as described previously (23). Five-microgram protein aliquots of the suspension were incubated at 37°C for 15 min in 50 mM Tris · HCl (pH 7.6) (containing 1 mM isobutyl-1-methylxanthine, 1 mM GTP, 0.5 mM ATP, 15 mM creatine phosphate, 80 μg/ml creatine phosphokinase, and 4 mM MgCl2) and 1 μM natriuretic peptides (NPs). Incubations were stopped by the addition of 375 μl of cold 50 mM sodium acetate (pH 5.8) and boiling for 5 min. Samples were then centrifuged at 10,000g for 5 min at 4°C.
RIA of cGMP.
The amount of cGMP generated in the supernatant was measured by equilibrated RIA (23, 28). To prepare iodinated cGMP, we used 2′-O-monosuccinylguanosine 3′,5′-cyclic monophosphate tyrosyl methyl ester (cGMP-TME; Sigma Chemical, St. Louis, MO). Iodinated cGMP-TME was made using the chloramine-T method and purified by a QAE Sephadex A-25 column (Sigma Chemical) (28). The specific activity of the iodinated tracer determined by the RIA technique was 215 Ci/mmol (18). Antiserum for cGMP was purchased commercially (Calbiochem-Novabiochem, San Diego, CA). Standards or samples were introduced in a final volume of 100 μl of 50 mM sodium acetate buffer (pH 4.8), and 100 μl each of diluted cGMP antiserum and iodinated cGMP were added. After incubation at 4°C for 24 h, the bound form was separated from the free form by charcoal suspension. Nonspecific binding was <2.4%. The 50% intercept was at 0.74 ± 0.03 pmol/tube (n = 10). The intra- and interassay coefficiency of variation was 4.2% (n = 15) and 7.1% (n = 8), respectively.
Competitive RT-PCR.
Left atria from 2- and 8-wk-old groups were immediately removed, put into liquid nitrogen, and kept at −70°C until assayed. RT-PCR was performed as described previously (21, 23). Total RNA was extracted from atria using TRI reagent (MRC, Cincinnati, OH), according to the manufacturer's suggested protocol. Total RNA concentrations were quantitated by ultraviolet spectrophotometry. One microgram of mRNA was suspended in 20 μl RT buffer containing 10 mM Tris (pH 8.3), 50 mM KCl, 5 mM MgCl2, 1 mM each of dATP, dCTP, dGTP, and dTTP, 20 U RNase inhibitor, 2.5 μM random hexamers, and 150 U Moloney leukemia virus RT (Perkin Elmer, Branchburg, NJ). mRNA was reverse transcribed at room temperature for 10 min and 42°C for 30 min. The reaction was stopped by heat inactivation for 5 min at 99°C and then chilled on ice. cDNA products were amplified by PCR with the following sense and antisense primers: NPR-B sense, 5′-AACGGGCGCATTGTGTATATCTGCGGC-3′ (730–756); NPR-B antisense, 5′-TTATCACAGGATGGGTCGTCCAAGTCA-3′ (1395–1421); NPR-B competitor sense, 5′-ATTTAGGTGACACTATAGAATACAACGGGCGCATTGTGTATATCTGCGGCGTACGGTCATCATCTGACAC-3′; and NPR-B competitor antisense, 5′-TTTTTTTTTTTTATCACAGGATGGGTCGTCCAAGTCAGCGTGGAGTATTACGAAGGTG-3′.
The NPR-B RNA competitor was made according to the manufacturer's suggested protocol (competitive DNA construction kit and competitive RNA transcription kit, Takara). Fifty microliters of PCR buffer contained 10 mM Tris (pH 8.3), 50 mM KCl, 2 mM MgCl2, 200 μM each of dATP, dCTP, dGTP, and dTTP, 2.5 U Taqpolymerase, and 1.5 pM each of sense and antisense primers for NPR-B and different concentrations of the NPR-B competitor (106, 5 × 106, 107, and 108copies). The temperature profile of amplification consisted of 30-s denaturation at 95°C, 1-min annealing at 58°C, and 2-min extension at 72°C for 40 cycles. PCR products (692 bp for NPR-B, 454 bp for the competitor) were separated in 3% agarose gels, and bands were visualized by ethidium bromide staining. Photographs of gels were taken, and the density was analyzed using a densitometer. The concentration of NPR-B mRNA was estimated by the amount of competitor at which the ratio of NPR-B and its competitor density was 1.
Statistical analysis.
The results are given as means ± SE. The significance of differences was determined with Student's paired and unpairedt-test. ANOVA followed by the Duncan multiple range test (see Fig. 2) was also applied. The correlation coefficients were determined using least-squares linear regression analysis, and the comparison of slopes was performed by a parallelism test. Statistical significance was defined as P < 0.05.
Characteristics of stretch-induced ANP secretion in 1-wk-old rabbits.
The basal rate of ANP secretion and ECF translocation was 0.79 ± 0.31 pg · min−1 · g−1 and 4.59 ± 1.13 μl · min−1 · g−1(n = 11), respectively (Fig.1, C and D). When atrial pressure was increased from basal level to 1, 2, 4, or 6 cmH2O for 4 min by the elevation of the outflow tip and then decreased to basal level, atrial volume (DRV) was increased by 159.9 ± 22.4, 227.9 ± 36.6, 302.2 ± 50.7, or 434.3 ± 78.4 μl/g, respectively (Fig. 1 B). The secretion of ANP was increased after reduction of atrial volume from stretch with peak values of 1.22 ± 0.42, 1.27 ± 0.45, 1.69 ± 0.46, and 5 ± 1.60 ng · min−1 · g−1 (Fig.1 C). The translocation of ECF was also increased by stretch at the same period as ANP secretion with peak values of 8.46 ± 2.22, 10.25 ± 2.11, 13.90 ± 3.48, and 17.44 ± 4.54 μl · min−1 · g−1 (Fig.1 D).
Postnatal changes in ANP secretion and ECF translocation.
Figure 2 shows changes in tissue weight and ANP content of left atria, DRV, ECF translocation, and ANP secretion from isolated perfused atria in response to increased intra-atrial pressure by 6 cmH2O in rabbits of different ages. Mechanically stimulated ECF translocation and ANP secretion were calculated by subtracting the mean value of the previous two observations from the peak value. Atrial weight gradually increased with age (Fig. 2 A). The tissue ANP content in the left atria was markedly increased from 0.65 ± 0.16 μg at 1 wk to 1.46 ± 0.25 μg at 2 wk and reached the peak value at 3 wk (Fig.2 B). DRV gradually increased and reached the peak value at 4 wk (Fig. 2 C). Mechanically stimulated ECF translocation and ANP secretion markedly increased with age and reached the peak value at 4 wk (Fig. 2, D and E). There were positive correlations between DRV, mechanically stimulated ECF translocation, and ANP secretion in all groups (Fig. 3). The leftward shift of these relationships with age happened suddenly between weeks 3 and 4, coincident with a marked increase in both ECF translocation and ANP secretion (Fig.3 B).
Postnatal changes in inhibitory effect of CNP on ANP secretion.
To evaluate postnatal changes in inhibitory effect of CNP on stretch-induced ANP secretion, we tested isolated perfused nonbeating atria from rabbits of three different ages (2, 4, and 8 wk old). Figure4, A and B, shows positive correlations between DRV and mechanically stimulated ECF translocation (y = 0.04x + 5.03;r 2 = 0.49; P < 0.001; Fig.4 A) and mechanically stimulated ECF translocation and ANP secretion (y = 0.11x − 0.34;r 2 = 0.44; P < 0.005; Fig.4 B) in control atria from the 2-wk-old group. CNP caused a slight increase in ANP secretion. Therefore, the relationships between stretch-induced ANP secretion and ECF translocation (y= 0.14x − 0.04; r 2 = 0.54;P < 0.001; Fig. 4 B) shifted leftward with CNP. In the 4-wk-old group, CNP did not cause any significant changes in relationships between DRV, ECF translocation, and ANP secretion (Fig. 4, C and D). In the 8-wk-old group, however, CNP caused suppression of stretch-induced ANP secretion. The relationship between ANP secretion and ECF translocation (y = 0.87x + 2.08;r 2 = 0.61; P < 0.001 in control group) shifted rightward with the addition of CNP (y = 0.59x − 0.79;r 2 = 0.85; P < 0.001; Fig.4 F), and a significant difference in the slopes (P < 0.05) existed. Therefore, as shown in Fig.5, the stretch-activated ANP in terms of ECF translocation (ANP concentration in the interstitium) was markedly suppressed by CNP in the 8-wk-old group but not in the 2- and 4-wk-old groups.
To determine whether the different age response of ANP secretion to CNP may be due to the amount of cGMP production, we evaluated the response of ANP secretion to 8-bromo-cGMP, a cell-permeable cGMP. As shown in Fig. 6, an increase in ANP secretion in response to given pressure was reproducible. 8-Bromo-cGMP (10−4 M) caused a marked suppression of stretch-induced ANP secretion in 2- (Fig. 6 A) and 8-wk-old groups (Fig.6 B). Therefore, ANP concentration was markedly suppressed in both groups (Fig. 6 C).
Postnatal changes in particulate GC activity.
To evaluate postnatal changes in GC activity in cardiac atria, we measured the amount of cGMP production stimulated by NPs in tissue membrane fractions of left atria. As shown in Fig.7 A, ANP, BNP, and CNP (10−6 M, n = 3) caused increases in cGMP production, which gradually increased with age. In particular, CNP-stimulated cGMP production showed a remarkable increase with age. Therefore, we evaluated the responsiveness of cGMP production using different doses of CNP in atrial tissue membranes from 2- and 8-wk-old groups (Fig. 7 B). Basal cGMP production in the 2-wk-old group was 15.53 ± 2.78 pmol · min−1 · mg protein−1(n = 7), which was higher than in the 8-wk-old group (8.87 ± 1.15 pmol · min−1 · mg protein−1, n = 7, P < 0.005). In the 2-wk-old group, the addition of CNP at doses of 10−10, 10−9, or 10−8 M did not significantly increase cGMP production. CNP at higher doses of 10−7 or 10−6 M increased cGMP production from 16.98 ± 3.12 to 19.12 ± 3.33 (P < 0.05) or 20.26 ± 3.67 pmol · min−1 · mg protein−1 (P < 0.01), respectively. However, in the 8-wk-old group, cGMP production was significantly increased by the lowest dose of CNP, and CNP-stimulated cGMP production was dose dependent. Therefore, the ratio of cGMP production by CNP to the control value was higher in the 8-wk-old group than in the 2-wk-old group (Fig. 7 B).
Postnatal changes in NPR-B mRNA.
To determine whether the different response of ANP secretion to CNP in young rabbits may be due to the lack of NPR-B mRNA, NPR-B mRNA in the left atrium was measured in 2- and 8-wk-old rabbits using competitive RT-PCR. By increasing the NPR-B competitor from 106 to 5 × 106, 107, or 108 copies, the PCR product of NPR-B was gradually decreased (Fig.8). The amount of NPR-B mRNA in the 2-wk-old group was not significantly different from the 8-wk-old group (n = 3).
The present study clearly shows postnatal changes in atrial compliance, stretch-activated ANP secretion, and GC-B activity and in the intracardiac role of CNP on the regulation of ANP secretion in rabbits.
It has been reported (30, 39) that atrial ANP mRNA and its content gradually increase after birth but ventricular ANP and its content abruptly decrease, although the mechanisms involved for the tissue-specific regulation of ANP expression are not well defined. To evaluate the responsiveness of ANP secretion to atrial stretch during development, we measured atrial compliance and stretch-activated ANP secretion in 1-, 2-, 3-, 4-, and 8-wk-old rabbits, using isolated perfused nonbeating atria. In the 1-wk-old group, increases in atrial volume induced by increased atrial pressure caused proportional increases in ECF translocation and ANP secretion, which have a close relationship, as previously shown in adult rabbits (5, 6). This means that ANP released from atria in response to stretch is secreted sequentially into atrial lumen along with the translocation of ECF in 1-wk-old rabbits. Atrial compliance increased progressively with age and reached the peak value at 4 wk (3.7-fold increase compared with 1-wk-old rabbits). Increases in atrial volume caused increases in ECF translocation in all age groups, which reached the peak value at 3 wk (3-fold increase, compared with 1-wk-old group). Postnatal changes in stretch-induced ANP secretion were more prominent than those in atrial volume and ECF translocation (30-fold increase compared with 1-wk-old group). Additionally, the leftward shift of ANP secretion in terms of ECF translocation with age happened suddenly between weeks 3 and 4 even though atrial ANP content had already reached the peak at 3 wk. The accentuated response to stretch of ANP secretion may be partly due to developmental changes in body fluid metabolism or endogenous stimuli of ANP secretion. Therefore, it is very likely that the age-related increase in ANP secretion was due to increases in atrial compliance and atrial ANP content.
The natriuretic peptide family and their receptors have been found in atrial myocytes and fibroblasts (15, 28, 29, 31). NPR-B (GC-B) is expressed in atrial tissue (28). In the present study, we found that cGMP production by CNP was attenuated in younger rabbits and increased markedly with age. These results suggest that CNP-NPR-B signaling in cardiac atria is developmentally regulated. Recently, we (28) reported intracardiac cross talk between ANP and CNP, showing the negative regulation of ANP secretion by CNP in beating rabbit atria, and an absence of the inhibitory effect of CNP related to the low activity of the GC-B enzyme in hypertrophied atria (22). The above results suggest that the physiological effect of CNP may change with age. Therefore, to define postnatal changes in the inhibitory effect of CNP on ANP secretion, we evaluated the effect of CNP on the ANP secretion from isolated perfused nonbeating atria from 2-, 4-, and 8-wk-old groups. Interestingly, an inhibitory effect of CNP was observed in the 8-wk-old group but not in the 2- and 4-wk-old groups. In the 2-wk-old group, CNP caused an increase in ANP secretion. At present, we do not know why the effect of CNP on ANP secretion changes with age. The amount of cGMP production from atrial tissue membranes was significantly higher in the 8-wk-old group than in the 2-wk-old group. However, NPR-B mRNA was not significantly different in both groups. Therefore, we conclude that the inhibitory effect of CNP on atrial ANP secretion is developmentally regulated, being absent during normal cardiac development in young animals and intact in adult animals. These data also suggest that the absence of the inhibitory effect of CNP on ANP secretion in younger rabbits may be partly due to low responsiveness of GC-B to CNP.
What is the physiological significance of postnatal changes in CNP-stimulated cGMP production and the intracardiac effect of CNP? The presence of an atrial CNP system suggests the importance of the intracardiac role of the CNP system as well as the ANP and BNP systems. CNP has a similar structure to ANP and BNP, but its functions are quantitatively different. Currently, endogenous CNP is known to influence the proliferation of cardiac fibroblasts (7), cardiac contractility (1, 28), and the secretion of atrial ANP (28). Cardiac hypertrophy is observed in transgenic mice lacking NPR-A (32). However, there has not yet been a study on transgenic mice lacking NPR-B. Recently, we (22) found low activation of GC-B by CNP without a difference in mRNA level in hypertrophied atria. Taking into account all the above data, there appears to be a relationship between NPR-B and cardiac hypertrophy and development. We suggest that GC-B activity may be kept low during the rapid growth period of the heart and then increase with the inhibition of cardiac growth. Increases in ANP secretion due to the absence of the inhibitory effect of CNP may contribute to the regulation of vascular smooth muscle tone to reduce cardiac overload during cardiac development. In contrast, ANP may also contribute to the regulation of cardiac hypertrophy to inhibit the proliferation of cardiac myocytes and fibroblasts. The latter effect of ANP is in opposition to the developmental changes caused by CNP. This may be due to quantitative differences or developmental changes in the functions of ANP and CNP. More study is required to fully understand the physiological role of cross talk between ANP and CNP systems in the cardiac development.
We thank Kyung Sun Lee and Sook Jeong Lee for technical help and Kyong Sook Kim for secretarial assistance.
This work was supported by Korea Research Foundation Grants KRF-99-042-F00022 F304 and KRF-2000-015-FP0023.
Address for reprint requests and other correspondence: S. H. Kim, 2-20 Keum-Am-Dong-San, Dept. of Physiology, Medical School, Jeonbug National Univ., Jeonju 561-180, Korea (E-mail:shkim{at}moak.chonbuk.ac.kr).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
- Copyright © 2002 the American Physiological Society

subset: commoncrawl


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ITALY: Rogue transporter strike could shut second Fiat plant
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'Dementia epidemic biggest challenge of the future': Lyketsos
Australian Broadcasting Corporation
Broadcast: 22/09/2009
World expert in dementia, Dr Constantine Lyketsos, is in Australia for dementia week. He contends that while big strides are being made in dementia research particularly on Alzheimers the money is being spent in a piecemeal way and governments are doing far too little to tackle one of the biggest health challenges of the future.
TranscriptKERRY O'BRIEN, PRESENTER: It seems the world is facing an epidemic of dementia, an epidemic Australia will not escape. There are a quarter of a million Australians suffering dementia today, a number that will double by 2030 and reach a million by 2050. If you're at the younger end of the age scale, that might seem like a long way away, but the clock is ticking. The problem multiplies when you consider how many carers will be required to look after those suffering dementia.
The world expert in dementia, Dr Constantine Lyketsos, is in Australia for Dementia Week, speaking at the National Press Club tomorrow. He contends that while big strides are being made in dementia research, particularly on Alzheimer's, the money is being spent in a piecemeal way and governments are doing far too little to tackle one of the biggest health challenges of the future. Dr Lyketsos is a professor in Alzheimer's disease research at the prestigious Johns Hopkins University in Baltimore, and I spoke with him in Sydney today.
Constantine Lyketsos, you talk about society facing extraordinary consequences from the rapid growth in dementia that's now being forecast. Why are the social consequences any more impactive than say heart disease or cancer?
CONSTANTINE LYKESTSOS, DEMENTIA EXPERT: Well, there are a couple of reasons for that. One reason is the sheer number of cases which are going to happen in a fairly concentrated period of time. The second reason is that dementia really is a chronic condition where the disability is sustained day in, day out for many years, whereas people with heart disease, the disability is intermittent and they're usually able to work. And the other reason in because the care needs of people with dementia pretty much always require one or more people around them to help them. So there's a multiplier effect in families.
KERRY O'BRIEN: You say that, with dementia, damage can be happening for years, if not decades, before the symptoms become apparent. What progress is being made in identifying dementia early on?
CONSTANTINE LYKESTSOS: The progress that's being made is what we call the biomarker effort. I prefer, actually, to call it a biological signature effort. The idea is that what's going on in the brain can be picked up by things like PET scans, MRIs, maybe blood tests or other tests that would tell us what's going on in the brain, how bad it is, how it's changing and so forth.
KERRY O'BRIEN: Question is: when do you start looking? I mean, how do you tell the difference between a memory that's in natural decline as part of the ageing process and a memory loss that might be a symptom of dementia?
CONSTANTINE LYKESTSOS: Well right now, we really don't encourage people to seek medical attention until there's a clear effect on their functioning, until their condition is impacting their ability to live alone, to drive, to look after themselves and so forth. But in the future, you might want to be thinking of this more along the lines of trying to detect, like we would in breast cancer, an early tumour, and to be able to do something about it.
KERRY O'BRIEN: Well how far away is that, because I know at the moment, for research purposes at least, there's a kind of one-stop shot; there's a two hour test you talk about, scanning test, which can scan across a range of possible symptoms?
CONSTANTINE LYKESTSOS: Right, so the two hour assessment includes several tests - PET scans, MRIs and so forth. The use of this clinically is several years away, because it's going to depend on validating them, and by that I mean us understanding the predictive value of the different tests. For example, there are PET scans now that can measure amyloid in the brain of people whether they have symptoms of dementia or not. The question becomes: if I take a normal person in their 70s and I do one of these PET scans, what does that information tell me for their future? In a woman who has a mammogram, if we detect a tumour, we might go down the path of doing a biopsy and that then tells us something about a treatment or a prognosis. So before we use the equivalent tests for dementia widely clinically, we need to figure out what the value is of the information that we're getting through validation.
KERRY O'BRIEN: So when you talk about the amyloids, you're talking about the synapses, aren't you? You're talking about the coating of the connection between the nerve cells?
CONSTANTINE LYKESTSOS: The amyloid refers to a protein that clumps in the brain. And you're right that it clumps close to the synapses and it makes the synapses fall apart and not work very well. But the amyloid itself probably is not a normal structure, so our ability to do a PET scan to see how much there is is telling us something about the disease of Alzheimer's starting in the brain.
KERRY O'BRIEN: What is the pathology of Alzheimer's, the simple pathology? It's pretty much what you're talking about.
CONSTANTINE LYKESTSOS: Right. There are three key elements. One are these plaques that deposit. The other is inside the nerve cells, which are the working end of the brain. We see things that we call tangles. And then the third major hallmark is the nerve cells die, and actually the death of the nerve cells in the brain are the ones that really predict the symptoms. So it comes in stages. You'd probably get amyloid first, probably get tangles after that and then later the nerve cells die.
KERRY O'BRIEN: But when you say that damage can be occurring for years if not decades before the symptoms become apparent, are you talking about a process that can be going on in a person in their 40s, in their 50s, or are you talking about 60s, 70s, as a norm?
CONSTANTINE LYKESTSOS: It very likely 60s, 70s, and possibly 50s as well. There have been studies of people who are at genetic risk for Alzheimer's, who've had some of these PET scans in their 40s and 50s, and they are showing PET scan pictures very similar to what people have much later who have early dementia. Whether that means that their brains are living with that pathology for many years or whether they're sort of almost immediately transitioning, we don't know yet.
KERRY O'BRIEN: So what real progress is being made for an effective treatment for Alzheimer's, if not a cure?
CONSTANTINE LYKESTSOS: Well over the last 10 years, the field has bet on this idea that amyloid is the driving force, so the progress that's being made is developing treatments that somehow remove or change the effects of amyloid on the brain. And these come in the form of pill or injectable medications called sigretace (phonetic spelling) inhibitors and they come in vaccine versions of treatments, usually injectable. And all of those now, and they're many, are being tested in clinical trials to see how and whether they help people with dementia. If the bet that amyloid is the driving force turns out to be correct, we will celebrating before the decade is out
KERRY O'BRIEN: But these things also throw up side effects, don't they?
CONSTANTINE LYKESTSOS: They can throw up some serious negative side effects. We are manipulating brain systems that we don't full understand, and when you do that you often get side effects that you don't expect. So when we enter people in trials, one of the things we tell them is that there are many unknowns and they might actually be putting their lives at risk for trying these treatments.
KERRY O'BRIEN: While we're waiting for the breakthroughs in research, you say that with determination we can reduce the prevalence of dementia and improve the quality of care. How?
CONSTANTINE LYKESTSOS: Reducing the prevalence probably has to do with knowing what the major risk factors are. So people who look after their health, especially manage their blood pressure, make sure that if they have diabetes or high glucose in their blood, that they manage that. People who try to keep active socially, who remain engaged, who keep their mind active and physically doing all of that probably will reduce the incidence of dementia.
KERRY O'BRIEN: You obviously feel that governments aren't throwing enough weight behind dementia research or even efforts to identify the onset. Do you think that that is because there's a tendency in society to by somewhat fatalistic about the fact that it's just one of the risks of growing old?
CONSTANTINE LYKESTSOS: That's a good question. I've never been good at understanding the minds of why governments make decisions or don't.
KERRY O'BRIEN: Well it's usually because of the pressure or lack of pressure coming from the public at large.
CONSTANTINE LYKESTSOS: Right. But there's one thing I would say in this point: the dollars, if you will, that it will cost us to find the cure for Alzheimer's disease are probably finite. I can't quite estimate them. I've heard people say US$20 billion, US$30 billion. Right now, we're spending these piecemeal, a little bit, a year at a time. And if it is $20 billion, then we're not spending it fast enough to really change the impact the disease is gonna have. So, I'd like to accelerate and front-load the spending of dollars that go into cure- related research.
KERRY O'BRIEN: You also clearly feel that not enough is being done on the side of caring.
CONSTANTINE LYKESTSOS: That's right. We know how to care for dementia patients and their carers right now. And there's good evidence to suggest that the care package we call "dementia care" helps not only their quality of life, but it helps the quality of life and health of the carers and also helps people age in place, whether it be at home or lower level facilities that they might live in. And yet, most people aren't benefitting from that. So the translation of dementia care to as many people as possible, while we're waiting for the cure, is for me a major priority.
KERRY O'BRIEN: Costos Lyketsos, thanks very much for talking with us.
CONSTANTINE LYKESTSOS: It's my pleasure. Thanks for having me.


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|By Mageddon725
|More from Mageddon725
|To the Fire Nation
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Book 1
Chapter 15
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Chapter 15: To the Fire Nation
Earth Rumble VI was in full swing. With the War over, more Earthbenders had come to challenge the reigning champion, the Blind Bandit. Toph, however, was bored. As she fought her opponents, even more than one at a time, she couldn't help feeling empty. This isn't fun anymore; I used to enjoy this.
The Boulder and the Hippo were trying to take her down as a duo, but they had just as much luck as the first time. Toph could feel their every movement and countered every attack with flawless precision.
"The Boulder and the Hippo will bury you!" The bulky Earthbender cried.
"Hippo mad!!"
Toph couldn't even laugh at them. "I'm so bored." She said under her breath. They launched two large rocks, but the projectiles had a small space in between. Toph merely had to turn sideways to dodge, and she sent two separate fissures toward her opponents. The Boulder was launched out of the arena when the fissure reached him, but the Hippo was partially submerged. Toph then flicked her hand out and sent the challenger out of the ring as well.
Xin Fu moderated once more. After being freed from his makeshift prison by some passerby, he decided to return to hosting Earth Rumble VI. "Ladies and Gentlemen, I give you your reigning champion, the Blind Bandit!"Toph smirked. At least victory still tasted sweet. That's when she felt three familiar sets of footsteps. "Twinkle Toes?" The Blind Bandit turned toward where they stood at the end of the stage.
"Hey Toph, how's it going?" Aang asked.
"I've never been more bored in my life!" She felt Katara and Sokka standing behind Aang. "Well, are you guys just gonna stand there or what?" They climbed up onto the stage and embraced their friend.
After Toph collected all of her things, the four of them exited the arena, and she told them how things had been. "My parents aren't overprotective like they used to be; they're still overprotective and all, but... you know, they're my parents. At least Gaoling knows that I exist now."
"That's great, Toph; I'm so happy for you!" Katara exclaimed.
"Yeah, well, it has gotten a little boring around here." She grinned mischievously. "I hope you guys aren't just here to talk."
"Well..." Aang began.
"Let me stop you there, Twinkle Toes—!" She glared at Sokka as he interrupted.
"Still not manly..."
She poked him. "Quiet you. Anyway, I want in. I don't care what you're up to; I want in."
"Great! We're headed to the Fire Nation to see Zuko." Aang said.
"Suki and the other Kyoshi Warriors will meet us there." Sokka explained.
Toph's inclined her head. "Suki's gonna be there, too, huh?"
"And don't forget Yun." Katara interjected.
Aang's eyes widened. "Oh, yeah! We met this Earthbender named Yun Zhen on Kyoshi Island; he's coming, too."
"An Earthbender?" Toph smiled; she might just have a rival. "What are we waiting for? Let's go!"
Yun awoke at dawn, as usual, but found that it was difficult for someone to perform any kind of meditative exercises on a boat. He did not have to wait long for the other warriors to come out of their quarters. Ty Lee walked over to him.
"Hey, I wanted to talk about last night."
Yun nodded. "So do I."
"I want us to be friends, Yun. I don't want you to feel like I'm your enemy."
"You're not," he replied. "I promise. I just--it's going to take some getting used to. I've hated the Fire Nation for six years..."
Ty Lee grinned. "But you don't hate me anymore?"
The Earthbender shook his head and smiled. "No, I don't. I couldn't if I wanted to; you're so nice and sweet that I can't even imagine why I hated you in the first place."
Both of them blushed as the moment passed, interrupted by Suki. "Look alive, people! Whale Tail Island is dead ahead!"
Yun saw the massive island, but he was distracted by smoke coming from far off in the distance. Yun shrugged; it was probably on another island.
"When we hit port, we are going to move to the airship that will take us to the Capitol. Any questions? No? Good."
Yun gathered his belongings: his sword, a pack with clothes, and a small bag of rocks for Earthbending on the go. "I'm ready.""Good." Suki said. "Because there's our ride."
"Oh boy..." Yun said as he looked at the massive hunk of metal.
The Next Day
Zuko looked down on the courtyard, preparing himself for yet another War Meeting. This one had been called by General Shu, and he did not know why. I hope it's not another challenge. Not that he couldn't handle himself, but Zuko was tired of the plots. War Minister Qin daily tried to press him into aggressive action of any kind.
Zuko laughed. "I guess with no war, he would get pretty bored." This recent call was troubling, though. Like Shinu, Shu was not a cruel man, and he had experience. Whatever got him to ask for this meeting was bound to require the aid of Aang and his friends. "Hopefully, they get here sooner than later."
The War Meeting came, and Zuko once again sat on his throne. "Why did you call this meeting, General Shu?"
The man in question stood. "I have pulled my men out of the Southern Earth Kingdom, as you requested, but there have been some... issues with the Earth Kingdom military."
Zuko leaned forward. "What kind of issues?"
"They have begun taking back the Colonies forcefully, ruthlessly even. They've killed our colonists and destroyed their homes. We believe that action should be taken." He indicated the other officers.
The Fire Lord frowned. "That doesn't sound like Kuei or any of the generals at all."
"That is why this is troubling; we've never seen such viciousness from them."
Zuko nodded, deep in thought. "I will be meeting with King Kuei in a week at Ba Sing Se; I will see what he knows. We can hopefully come to an agreement or resolution then."
Shu glanced at the others. "What should we do in the mean time?"
Zuko rubbed his temples. "Send small contingents, and I do mean small, to each Colony to aid them. Once this is sorted out with Kuei we can simply remove them again."
"As you wish, Fire Lord Zuko."
Team Avatar rode toward Capitol Island with the wind at their backs. "We're making great time!" Aang exclaimed.
"Hey, Aang, when is that big meeting with all four nations again?" Katara slid up beside him.
"In about a week Kuei, Arnook, Hakoda, and Zuko will all be there. It is being held in Ba Sing Se."
Sokka pointed his sword at Aang. "Aren't you supposed to be there too?"
"Yeah, I was told that it was the Avatar's duty to be there, and there hasn't been one of these since the War started."
Toph chimed in. "That should be exciting for you, meeting with all of those important people. But what about us?"
Aang shrugged. "I don't know. You guys could go visit Iroh at the Jasmine Dragon."
"I guess so..." Toph blew her hair out of her face. "But you still have the coolest things happen when we're not around!"
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It is not the beautiful women who have spiced his life that most bring a smile to the face of Ronaldo, nor the choice of the worlds finest automobile products (although Monday he was driving a modest Alfa after someone pinched his race-machine of a BMW). Real Madrids lively striker admits to even greater thrills than when one of his outlandish golfing gambles pays off.
Ronaldos features flicker most with delight when he runs at a friend in training, drops a shoulder to feint movement in one direction, so forcing his opponent to stretch his legs and present an enticing gateway. After guiding the ball through, Ronaldo darts around, chuckling at a successful nutmeg.
The Brazilian is always playing games in training, always attempting to lure highly-competitive defenders like Reals accomplished right-back, Michel Salgado, into a trap so he can whisk the ball past him with a flourish.
If he nutmegged Salgado in training that would be it for Ronny, said his close friend and clubmate, Steve McManaman, on Monday.
Ronny would walk off, happy in the knowledge that he has got something over on somebody and done some trick that worked.
The pleasure principle was learned early as a child raised revelling in the balls potential for making fun of an opponent, the code of the beach or playground. The doctrine was strengthened by brutal acquaintance with adversity, notably the panic attack before the final of France 98 and then the years lost to a knee injury that many thought would remove this wonderful panther of a centre-forward from the game forever.
Ronaldos return to form at Korea-Japan 2002 was the stuff of fairytales, earning him global adoration and a move from Inter Milan to Real.
Charged with casting the English vote for European Footballer of the Year, this observer chose Roberto Carlos for an unstinting succession of high-octane displays for Real and Brazil. But Ronaldo waltzed away with the award and, in truth, it was hard to begrudge him the honour.
In a sporting world where self-aggrandisement can run rife, Ronaldo assumes few airs. Observed in Brazils hotel on the eve of the Yokohama final, Ronaldo was all smiles, signing autographs and spreading a little happiness to those who had waited patiently for a glimpse of the man shredding defences for fun.
Ronaldo is mad in a happy-go-lucky way, always loud, always messing about, always trying to do jokes on people, McManaman said.
Spend an hour in his company and you come away thinking what a lovely bloke he is without understanding a word hes said. He makes gestures and is laughing all the time.
The Carnival has come to Castille.
Ronny is the most famous player on the planet yet hes not got an ego. I dont know how he stays sane with all the attention; when we went to Tokyo for the Inter-Continental Cup everybody recognised him from children to old ladies.
He enjoys it. Just as Ronaldo enjoys fames booty: the island off Brazil bought with a signing-on fee, the Porsches given to try out, the lessons with his golfing coach as he attempts to lower his handicap from 16.
McManaman occasionally picks up sticks with Ronaldo, slicing and laughing their way around Madrids premier fairways.
Ronaldo, typically, does not hold back. He just likes to smash the ball, McManaman added. And he wants to bet on everything. Hes a worse gambler than me. I bet you I can do the longest drive. I bet I can put it on the green. How much'!
Esteemed in the dressingroom, Ronaldos popularity with the Bernabeu public would be greater if he had not taken the place of the much-loved Fernando Morientes.
Ronaldo also spends games doing little, then bursting into prolific life, a contrast to the selfless, ceaseless involvement of a true Real legend, Raul.
Raul helps Ronaldo look good with the slide-rule passes cutting through back-lines for the Brazilian to run on to.
Where Ronaldo truly excels is his instinctive knowledge of where best to target his runs; he is blessed with the close control and acceleration over a short distance to make his selection of run even more devastating.
He is a smiling assassin lying in wait.


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Hi there, I'm DeeDee! I am a 4-year-old cockapoo looking for new humans to love. I am a pretty remarkable girl at only 15 pounds. Once I arrived to OBG, I found out from the doctors that my heart is significantly enlarged, and I need daily medications for my heart that costs around $100 per month and I need to go outside every couple of hours. The doctors explained that due to my condition, I only have a couple of years at most to enjoy life. I've decided to embrace life to the fullest and just be a happy girl. Please see the video link below of me doing just that!
Check out a cute video of Dee Dee here:
Now for the happy info - I am beautiful, sweet and get along wonderfully with other dogs. I love to greet everyone I meet, but when I'm alone, I can happily entertain myself with toys. But I do not want to be crated or even gated and will howl and cry in protest. Because I love my freedom, I would be okay with dog savvy children over 8. Oh and I love, love, love toys, and tennis balls are especially fun!!!
Do you work from home or have a doggie door? If so, I may be a good match! If so, please send an email at the link below.
A Little History: OBG originated in Northern Virginia in 1996, out of a concern for local senior dogs that found themselves without homes, and had virtually no options for being rescued. OBG now rescues cockers and cocker mixes of all ages, and has grown over the years to serve not only the Washington DC metro area, but also the Mid-Atlantic area. Year over year, we place around 300 dogs. We typically have around 75 dogs in our "inventory" which are kept in private foster homes.
If you have a interest in a specific dog, contact us. Not all our dogs attend each show.
Download our application form, fill it out and bring it to the show. That will save time!
Adoption shows are usually stressful for the dogs, so they are not necessarily all going to run up and lick you in the face and wag their tails like mad! Cockers are very attached to their owners, consequently at the shows they are typically trying to stay as close to their foster volunteer as possible and they may just politely ignore you. Don't hold this against them, all the love you see them showering on their foster volunteer will transfer to you very quickly.
If you already have a dog, you should bring it to the show to see how the two dogs interact. Dogs have opinions too, and the nicest dogs in the world may just decide that they don't like each other. Don't worry if the two dogs don't instantly fall over each other in a wagging licking frenzy. If they just do a courteous sniff and wag, and then wander away, that's fine. The point is to make sure they don't start growling and snapping at each other.
Adoption process: If you are interested in adopting a dog from us, we suggest that you first download the application form on our website and fill it out. Bring it with you to one of our adoption shows, and/or contact us to let us know of your interest. We also have an fill-in application form in MS-Word that you can fill in and email back to us. Based upon your application and conversations with you, we will make recommendations on which of our dogs might be a good fit. If a specific dog you are interested in is not available at an adoption show we can make arrangements for a private meeting with the dog and his/her foster mommy/daddy. Before you take your dog home we will perform a homecheck. We finalize the adoption with an adoption contract. The adoption fee is $350 for the first dog and $250 for the second dog, if adopted within 3 months of the first one. This fee helps pay for medical care, food, and shelter for the dogs.
*Note* We have a 14 day refund policy so that you can confirm that the dog is going to work out in your home - if it doesn't work out we can refund the money or work with you to find another dog. After the 14 day period, the fee is not refundable, but we can work with you to find another dog.
Thank You!
Your message has been sent to Oldies But Goodies Cocker Rescue, Inc..
You'll receive a copy, too, at to help you keep track of which pets you've inquired about, and which shelters and rescues you've emailed.
NOTE: Some shelters have physical locations you can visit; some of these shelters may only have pets for a limited time, so please do not wait for a reply—just go visit the shelter! Other organizations are rescue groups run by busy volunteers who may take a while to reply. You can find information about the shelter or rescue group caring for this pet, and their adoption procedures, on the pet's details page on Adopt-a-Pet.com.


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I just met a guy a few weeks ago and he wants to hangout. But I was thinking about suggesting to go hiking. Do you think that's weird? just because the typical first dates are like movies and dress up nice and looking good
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Hiking sounds like a great first date.00|00|0


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Duncan Wants Government Out Of (Private) Business
S.C. Rep. Jeff Duncan wants the government out of the private sector – and the Congressional candidate is looking to make a federal bill that does just that a centerpiece of his upcoming campaign.
It's called the "Government Ownership Exit Plan," and Duncan's advisors correctly deduced that it might appeal to us.
Sponsored by U.S. Sen. John Thune (R-South Dakota), the legislation would prevent the U.S. Treasury from purchasing any additional ownership stake in private companies using Bush bailout funds (which all four "Republican" Congressmen from S.C. voted for, we'd like to add), as well as require the Treasury to sell any current ownership stake in private firms by July 1, 2010.
It would also "re-privatize" failed government mortgage behemoths Fannie Mae and Freddie Mac, and explicitly prevent the government from making private sector management decisions.
"This legislation is filled with practicality and commonsense, both of which seem to be lacking in Washington these days," Duncan told FITS. "It is not the government's role to own businesses or to take American workers' hard-earned money in the form of taxation to invest in private companies. It is time for an exit strategy to this nonsense and the Government Ownership Exit Plan Act of 2009 sets the wheels in motion for this to take place by next year."
Frankly, it's sad that legislation like this is necessary in the United States of America, but such is life.
Anyway, Duncan sent a letter about Thune's bill to every member of the S.C. Congressional delegation, a letter you can read by clicking on the handy-dandy link below …


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The Sun!
Fatimah Abdullah
Earth Science - Period 7
Mr. Taylor & Mrs. Rapoport
How was the sun formed?
From studies of other stars, it seems pretty convincing from the data that the sun must have started out as a large collapsing cloud of gas inside some ancient interstellar cloud. This cloud was polluted by a supernova several million years before the collapse phase ended. The cloud collapsed for millions of years until it formed a rotating disk with a large central bulge. Out of the disk would eventually form the planets, and out of this central bulge where most of the mass wound up, formed the sun.
Your message...
When was the sun formed?
The sun was born roughly 4.6 billion years ago.
What chemicals make up the sun?
You see that hydrogen is by far the most abundant element in the Sun, followed by helium. Those two together make up 99.9 percent by number of the total atoms in the Sun!
What Is the Fusion Reaction That Occurs in the Sun?
The fusion reaction that occurs in the sun is called nuclear fusion. In physics, this is a situation where at least two nuclei of atoms bind with each to produce a much more heavier nucleus. Nuclear fusion is the type of nuclear reaction that powers all stars in the universe, including the sun.
When will the sun die out?
In approximately 5.5 billion years, the sun's gravity will no longer be able to hold its mass in. This is due to the constant loss of mass by the sun. It will expand greatly.
What is a dark spot on the sun ?
Sunspots are temporary phenomena on the photosphere of the Sun that appear visibly as dark spots compared to surrounding regions. They are caused by intense magnetic activity, which inhibits convection by an effect comparable to the eddy current brake, forming areas of reduced surface temperature.
How much mass does the sun have?
The Sun has a mass of 2,000,000,000,000,000,000,000,000,000,000 kg.That's 330,000 times the mass of the Earth.
What is the structure of the sun?
The sun has an interior and an atmosphere. The interior includes the core, the radiation zone, and the convection zone. The sun's atmosphere includes the photosphere, the chromosphere, and the corona.
What kind of star is the sun?
The Sun is a G-type main-sequence star (G2V) based on spectral class and it is informally designated as a yellow dwarf.
How does the sun get its energy?
The Sun produces energy by the nuclear fusion of hydrogen into helium in its core. What that means is that, since there is a huge amount of hydrogen in the core, these atoms stick together and fuse into a helium atom. This energy is then radiated out from the core and moves across the solar system.


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Blank Leather and Duck Cloth Hat // Black on Black
$ 58.00
The entire front panel and the top button of this hat are made of super soft Napa Valley Lambskin leather. The brim, side and back panels are constructed using 100% black cotton duck cloth and finished with black metal eyelets. This hat is adjustable to fit any size by a leather strap and metal clasp at the back. Made in the USA.


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Thursday, April 19, 2007
Was This The Best Music Video Ever?
Sorry, the YouTube imbedding was disabled, so you need to follow this link.
Maybe I'm just tired, but Warrant makes me smile. :) It's just too bad that the image quality is so bad. Oh well. Enjoy this fine song...
Posted by Steve Buccellato at 4:02 PM 9 comments:
Labels: Best Video Ever, Cherry Pie, Warrant
Friday, April 06, 2007
Mo' Manga Mayhem
Posted by Steve Buccellato at 10:42 PM 1 comment:
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Systems Administrator/Sr Field Engineer
Walnut Creek , California
November 15, 2016
Our East Bay client is searching for a Sr Field Engineer with a background in Systems Administration. Experience in Network support is a big plus! Must be willing to travel on a regular basis around the Bay Area and be comfortable working with multiple environments. If this sounds like you please contact Tara Sweatt at tara.sweatt@rht,com Duties and Responsibilities • Monitors system performance using built-in and 3rd party monitoring tools to ensure systems are healthy and meet desired service levels. • Routinely provides IT Operations Manager with system capacity reports showing historical trends and helps plan purchases and budgets. • Implements and maintains facilities and reporting infrastructure to continuously monitor system event logs using systems management tools such as MS MOM. • Installs new servers, equipment upgrades and enhancements and ensures systems are operationally ready and can be recovered before applications are installed and user can access the system. • Configures and provisions new virtual machines in VMware, ensuring the configuration is appropriate and complies with established standards and is well documented. Also provisions storage and backups as required.
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Founded in 1948, Robert Half (NYSE: RHI) is the world's first and largest specialized staffing services firm.
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Welcome to Storehouse, visual storytelling for the iPad. It's the easiest way to create, share, and discover beautiful stories. Combine photos, videos, and text to meaningfully document your experiences. Publish stories for friends and followers, and share them by email, Facebook, or Twitter. Explore stories from our community of storytellers from all around the world.
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For insurers that want a customized product without investing time and money in the research and development work of doing so, AAIS has the essential resources and people for the job.
Each of these steps is critical to developing a successful program, and each can be time-consuming and costly to those unfamiliar with the process.
By using AAIS programs and staff to manage the details of custom product development, your staff can concentrate on refining your underwriting and marketing strategies.
Insurance companies seeking more information on AAIS products and
services can contact Rick Maka, director of marketing and strategic
alliances, at our contact form , or by calling 800-564-AAIS, ext. 3222.


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Sixty six groups led by the American Energy Alliance sent a coalition letter this week to Speaker of the House John Boehner and Senate Minority Leader Mitch McConnell urging them to oppose the inclusion of the wind production tax credit (PTC) in any lame duck tax extenders package during the remainder of this congressional session. Click here to read the letter.
In the News
Dear GOP: Don't Rescue Obama Energy Policy with Wind PTC Extension
Robert Bradley, Jr., Master Resource, 7 November 2014
Enough of Big Ethanol Bullying Voters
Nan Swift, Washington Examiner, 7 November 2014
West Virginia's White, Pro-Coal Democratic Senate Candidate Fared Even Worse Than Obama
David Weigel, Bloomberg, 6 November 2014
GOP Election Rout Delivers Blow to U.S. Leadership Role on Climate Change
John Cushman, Jr., Inside Climate News, 5 November 2014
Obama: Stop Bugging Me About Keystone
Ben Geman, National Journal, 5 November 2014
Sierra Club's Wacky Take on the Election: Environmentalists Failed Due to "Sinister Voter Suppression Tactics"
William Yeatman, GlobalWarming.org, 5 November 2014
Climate Was Barely a Factor in Midterms
Brad Plumer, Vox, 4 November 2014
The Crazy Reason Two Auto Companies Were Fined $100 Million
Nicolas Loris, Daily Signal, 4 November 2014
News You Can Use
Election's Biggest Loser: Alarmism
Last week, the Cooler Heads Digest reported on the scores of millions of dollars that green special interests and their billionaire benefactors spent on the midterm elections. Regarding their efforts, this week's Politico headline delivers the final word: "Tom Steyer, Greens Have Rough Night at the Polls."
Inside the Beltway
Myron Ebell
Big Green's $85 Million Fails To Keep Senate under Harry Reid's Control
Republicans gained at least seven and probably nine Senate seats in the 4th November congressional elections and will take control of the Senate when the 114th Congress is sworn in on 3rd January. Senator Mitch McConnell, the current minority leader, defeated Alison Lundergan Grimes in Kentucky by 52 to 44% and will become majority leader. EPA regulations to kill the coal industry were a big issue in the campaign.
House Republicans increased their numbers to between 245 and 250 from 233 in the current Congress. With several races still to be called, the Republicans could hold more seats in the House of Representatives than at any time since 1929.
Republicans did this despite massive spending by billionaire green activist Tom Steyer and the big environmental pressure groups. As I reported last week, Big Green spent over $85 million trying to elect global warming alarmists. They failed miserably. Their issues did not resonate at all. As Republican pollster Whit Ayres said, "It is difficult to find an issue that voters place lower on the list than climate change."
Steyer and leading environmentalists have spent the week trying to explain away how they spent so much and achieved so little. But environmental advocates, such as Brad Plumer writing on Vox, were also quick to acknowledge that the global warming establishment was the biggest loser in the elections. Here's the good news from Rebecca Leber in the New Republic: "Congratulations, voters. You just made this climate denier the most powerful Senator on the environment." She refers to Senator James M. Inhofe (R-Okla.), who is set to return as chairman of the Environment and Public Works Committee.
In a press conference the day after the election, President Barack Obama admitted, "The Republicans had a good night." He then went on to say that he was not planning to make a mid-term course correction or shake up the White House staff, as did Presidents George W. Bush in 2006 and Bill Clinton in 1994. It's going to be an interesting two years in Washington, DC.
Across the States
Myron Ebell
Republicans Make Historic Gains in State Legislatures
The Republican takeover of the Senate was the big story on election night. A few days to look at the election results at the state level has convinced me that the stunning scope of Republican victories in state legislative races is at least as big a story and will have bigger consequences over time.
Republicans increased their control of the 98 partisan state legislative bodies (Nebraska's legislature is non-partisan and unicameral) from 57 to 67 (and after the election, a party switcher gave Republicans control of one more). Once all the races are called, it is almost certain there will be more Republican state legislators than the previous high of 4001 achieved in 1928.
Democrats lost their majorities in the West Virginia House for the first time since 1931. West Virginia's current House of Delegates has 54 Democrats and 47 Republicans. The new House will have 64 Republicans and 36 Democrats. After Democrats lost seven state Senate seats in West Virginia, a Democratic state senator announced that he would switch parties, which will give Republicans control of the state Senate, again for the first time since 1931. In New Mexico, Republicans won control of the state House for the first time since 1954.
Democrats also lost their majorities in the Nevada House and Senate, their Senate majorities in New York, Colorado, Maine, and Washington, and their House majorities in Minnesota and New Hampshire.
Before the election, Republicans controlled both legislative chambers and the governorship in 23 States, Democrats in 13. Republicans gained complete control in Nevada and Arkansas, but lost it in Pennsylvania (where incumbent Governor Tom Corbett lost) and Alaska (where an independent defeated incumbent Governor Sean Parnell). Democrats, on the other hand, lost complete control in six States: Maryland, Massachusetts, Minnesota, Colorado, Illinois, and West Virginia.
Thirty-One States Now Have Republican Governors
The biggest surprise on election night was Republican Larry Hogan defeating Democratic Lieutenant Governor Anthony Brown for Governor in Maryland. Republicans Bruce Rauner and Charlie Baker also won surprising victories for Governor in Illinois and Massachusetts.
Democrat Tom Wolf defeated Republican Governor Tom Corbett in Pennsylvania. Otherwise, it was a big night for Republicans at the gubernatorial level, who now have thirty-one Governors.
Democrats now have one woman Governor—Maggie Hassan in New Hampshire. Republicans have three—Susana Martinez in New Mexico, Nikki Haley in South Carolina, and Mary Fallin in Oklahoma. Democrats have no Hispanic Governors, but Republicans have two—Martinez and Brian Sandoval in Nevada. Republicans also have two Governors of Asian Indian descent—Haley and Bobby Jindal in Louisiana.
The Cooler Heads Digest is the weekly e-mail publication of the Cooler Heads Coalition. For the latest news and commentary, check out the Coalition's website, www.GlobalWarming.org.


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We just booked a cruise that leaves from Southampton on Nov. 30th. We are flying into LHR either one or two days prior to the cruise. Our flight would arrive at 7:05 am. We have never been to London before so am trying to sort everything out.
We are looking for a hotel in a reasonable price range (less than $300 per night, if possible). I am not sure what would be a good location for us to stay. We would like to do the Ho Ho bus tour of the city as we feel that is the best way to see the city w/ a limited amount of time.
I am looking for assistance in departing the airport to whatever hotel we book.
The next question I have is concerning how to get to the Southampton port for our cruise. I know that National Express runs to the port as well as trains but not sure which would be the most expedient way to get there. How early should we leave London for the trip to the port? We probably can't check in on the ship until at least 11 am or later.
Several people have suggested the train.
I am looking for advice from all you Fodorites who have been to London. Many thanks for your help.
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Need Help W/ London Lodging
We just booked a cruise that leaves from Southampton on Nov. 30th. We are flying into LHR either one or two days prior to the cruise. Our flight would arrive at 7:05 am. We have never been to London before so am trying to sort everything out.
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DOes your ship offer a shuttle?I know Cunard does, and it takes you right to docks. I would check that first.
We have made 2 trips a year to London for the last 40 years and I mrefer the South Kensington Glaocester rd area.wE STAY at the millenium gloucester or Millenium Baileys .quite nice large rooms and convenient transport. Never done the hoho bus as the reguler routes go all over and don't break the budget, Lots of good resturants in walking distance
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It seems a shame to me to visit London for just a day or 2. Presumably there's a reason for it but I suggest you apply yourself to not only these details but to the possibility that you'll be sorry when you realize (if you realize) what you'll be missing. You may love a good cruise but compared to a week or 2 in London it wouldn't hold a candle (in my opinion, of course).
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Avalon, I do not believe there is a shuttle to port unless you book a package deal w/ the cruise line which we didn't do. I will check out your suggested hotels. I am still acclimating myself to navigating London and it's transportation system. This is why I am looking for suggestions from those of you who have been to London b4. My most important thing right now is to book a hotel.
MmePerdu, couldn't agree more w/ your comments about only staying a couple of days. Everyone has their own favorite way of travelling, we happen to luv cruising and realize that we only see a very small portion of the particular country we visit. Cruising also gives us the opportunity to plan a return visit for a longer period of time after we have been in a port for a day or two.
There are reasons why we are unable to plan a longer visit to London, but for right now we are trying to find suitable lodging for our two- day visit and hope that others may have some suggestions for us.
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Most trains to Southampton leave from Waterloo station. Some leave from Victoria. So you would be better off staying near one of those.
If you have Marriott points (or can get a deal to fit it w/i your budget) the Marriott County Hall can't be beat. It is very close to Waterloo and has wonderful views of Big Ben/Parliament/the river/the Eye.
If points/a deal aren't doable - then the County Hall Premier Inn would be good. Not posh at all but clean/modern and the same general location as the Marriott (no views though since it is at the back of of the same complex). It would be well under your budget.
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We can recommend Cartref House B and B Hotel in Belgravia, a 10-minute walk from Victoria Station. Last October we took the tube from LHR to Victoria Station and walked to Cartref House. We travel light, so with more luggage, this may not be a practical option for you.
Check out Cartref House on Trip Advisor. Ground floor family room was decent size, small bathroom, good breakfast, helpful hosts, good price for London (127 GBP) and located in a quiet neighborhood. We are a couple, but chose the family room for the ground floor location and more space.
We've also stayed several times in South Kensington, but too long ago for hotel recommendations. If you prefer having the amenities of a large hotel, you probably won't be interested in the b and b experience.
Armed with a London guide book and a map, you will find the city easy to navigate either by bus or the tube or a combination of the 2. You may prefer the buses for the above ground scenery. Guide book will give you information on buying Oyster card to use on buses and the tube.
There are trains hourly from Waterloo Sta. to Southampton, a trip of about 1.5 hours. Cartref House can arrange a private transfer to Waterloo Sta.
"Visit Southampton" website has cruise ship/port information that may be helpful.
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If you want a longer visit to London foloowing a crise (rther a transatlantic crossing) I cannoy recommend more highly the QAueen Mary 2> I'd do it again in a heartbeat!!
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If it were me I would use Priceline to book a 4 or 5* hotel in Central London - so you can walk to a lot of sights. Have a look at Covent Garden, Mayfair, near Picadilly etc. Should be within your budget.
South Kensington isnt bad - but not as central.
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We returned via the Queen Mary last September after two weeks in Scotland and we didn't like it at all. After the first miserable evening/dinning experience (dining with several hundred people is not our idea of a good evening, service bordered on rude and food was cafeteria-like). We booked Todd English the next evening, and it was excellent. We went back the remaining nights. There were a lot of activities, but not all suit, and I walked out of one lecture it was so bad. The talks in the art gallery were very good as were several of the musical groups but overall a long 7 days. That said, we never thought of ourselves as cruise people but hoped this might be a good alternative to those seemingly long hauls westbound. Not for us, but if you like cruising it's probably a great experience.
Fodorites have offered several good recommendations for lodging. It just depends on which location you prefer...all mentioned are central.
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You must have had bad luck we had exceptional service . Our dinner companions were delightful, an English couple from the Lakes district ahich we are quite familiam r with and 2 American ladies who traveled extensivly. Our food at lunch and dionner was very good and the service was superior, There was lobster on the menu one night and my DH said he'd love to have that except one little tail didn't satisfy him, Tomas siad not to worry and brought 2nd helpings for sll of us!They could not have been mre helpful and polite.We are very early risers and had breakfast in the King's gallery with a plentiful buffet Scrambled eggs were on the line but if you wanted fired or poached they were freshly prepared for you .We especially enjoyed the pianist in the pub directly outside the dining room
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Historytraveler, I, too, was seriously disappointed by my week going home from the UK on the QM2. Similar criticisms plus others but suffice it to say it is, indeed, not for everyone.
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The Boonton High School wrestling team completed its unbeaten run through the Suburban Division of the Colonial Hills Conference last week to capture the division title it shared last year with Whippany Park.
Boonton (14-1 overall, 10-0 in the league) won three matches in four days - all in convincing style - as the Bombers defeated Glen Ridge, 52-15, last Wednesday; stopped Newark Academy, 65-10, on Friday; and routed Verona, 73-3, this past Saturday to officially clinch the division championship.
Matt Zienowicz, second in the Morris County Tournament at 189, improved to 23-2 on the year as he won twice by pin and once via forfeit.
Wesley McCombs improved to 17-4 with two pins and a forfeit; John Takacs is now 17-5 after registering three pins; Ray Milewsky had a pin and two decisions to improve to 16-6; and Mike Moussa improved to 16-5 with a pin, major decision and a forfeit victory.
Billy Beiermeister and James Arnest each won their 14th bouts of the season last week; Matt Rathbun won his 13th; and Jon Latona, off to a late start because of injury, improved to 13-2 with two pins and a tech fall victory.
Mountain Lakes
Mountain Lakes got the first wrestling victory in school history last Tuesday when it defeated Pingry, 42-33.
Eric Guadara, Jeremy Jones, Andy Plaisted, Ron Harrison and Rob Harrison posted pins in the Lakers (1-2) historic victory. Ray Funahashi and Dan Brennan won by decision and Doug Beck picked up a forfeit victory.
The Tigers of Dover lost their first six bouts to powerful Hanover Park last Wednesday to drop a 48-21 decision to the 15-1 Hornets.
Cesar Cordero, runnerup at 103 in the Morris County Tournament, won by a pin at 3:25 for Dover's only pin victory.
Jason Sosa won his bout at 125 on an injury default; Chad Jones decisioned Mike Torsiello, 9-8 in overtime of their bout at 140; and Ryan Coltelli (215) won by forfeit for the other Dover (8-5) victories.
Morris Catholic
Morris Catholic got its only points from pin victories by Alex Keith and Mark Ambrose as Madison dominated the Crusaders, 71-12, last Wednesday.
Keith pinned his 145-pound foe at 3:30 and Amborse got the better of his foe just 1:12 into their heavyweight match. MC is now 1-8.
Morris Hills
The Knights (6-10) dropped all three of their matches last week, losing a 58-21 decision to West Morris last Monday; falling to Mount Olive, 53-14, on Wednesday; then losing to sister-school Morris Knolls, 46-21, this past Friday.
Ray Sarinelli won all three of his bouts - two by pin and one by decision; James Curley was 3-0 with a pin, tech fall and a decision; and soph heavyweight Vin Lusardi picked up two decision wins and a forfeit victory.
Morris Knolls
Morris Knolls lost to Seton Hall Prep, 50-15, last Wednesday before turning the tables on sister-school Morris Hills, 46-21, on Friday.
Jim Zemzicki and Keith Deter got pin victories and Steve Senichka won by decision against Seton Hall.
Against Hills, Matt Herr, Chase Taylor and MCT runnerup Kris Cacella recorded pin victories. Jesse Doyle won a major decision and Deter and Carlos Alvarez registered decision victories.
Spencer Hollerith, John Petrozzino, R.J. Mount, Joey Filippo and Mike DeFillippo registered pin wins as Montville defeated Caldwell, 49-25, last Wednesday.


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Universal Plunger Switch
Part #: 31-9663
List Price: $8.57Our Price: $6.99
Plunger interlock switch replaces Ariens 27541, John Deere AM103119, MTD 725-3167, Murray 57211, Snapper 15707. Single post, right angle snap mounted. Normally open.
|OEM Replacement This part is aftermarket equipment designed to replace the original manufacturer's part numbers specified here. It is manufactured using high-quality materials, to the same specifications as the original part.
|Ariens 27541, John Deere AM103119, MTD 725-3167, Murray 57211, Snapper 15707, MTD 9253167, Murray 024273, AYP 160784, Roper 160784, Sears 160784, AYP 532160784, Roper 532160784, Sears 532160784


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David Lamka
- Quito, Ecuador
- orangeskyecuador.com
I was born in Switzerland and moved to Latin America in 2010, where I worked on numerous projects focused on humanizing the business world and creating spaces for all sectors of society to engage in meaningful and transformative dialogue. I continued my studies in 2012 in Ontological coaching in Chile and Transpersonal and Integral Coaching in Ecuador. Currently, I am a Professional Certified Coach by the International Coach Federation and dedicate a great deal of my time to life and organizational coaching. I am also an Art of Hosting and participative leadership facilitator, I facilitate dialogues, workshops on personal development, non-violent communication, and conscious entrepreneurship tools. I meditate since 2011 and I try to follow up with my wife's yoga classes since 2015.
My passions: Family, nature, South America, spirituality and retreats, building networks, meditation, conversations and generating change
My purpose: Accompany and facilitate people's development, consciousness, and healing processes
My focus: Personal and organizational development