text:
Renin secretion is regulated in part by renal nerves operating through β1-receptors of the renal juxtaglomerular cells. Slow sodium loading may decrease plasma renin concentration (PRC) and cause natriuresis at constant mean arterial blood pressure (MAP) and glomerular filtration rate (GFR). We hypothesized that in this setting, renin secretion and renin-dependent sodium excretion are controlled by via the renal nerves and therefore are eliminated or reduced by blocking the action of norepinephrine on the juxtaglomerular cells with the β1-receptor antagonist metoprolol. This was tested in conscious dogs by infusion of NaCl (20 μmol·kg−1·min−1 for 180 min, NaLoad) during regular or low-sodium diet (0.03 mmol·kg−1·day−1, LowNa) with and without metoprolol (2 mg/kg plus 0.9 mg·kg−1·h−1). Vasopressin V2 receptors were blocked by Otsuka compound OPC31260 to facilitate clearance measurements. Body fluid volume was maintained by servocontrolled fluid infusion. Metoprolol per se did not affect MAP, heart rate, or sodium excretion significantly, but reduced PRC and ANG II by 30–40%, increased plasma atrial natriuretic peptide (ANP), and tripled potassium excretion. LowNa per se increased PRC (+53%), ANG II (+93%), and aldosterone (+660%), and shifted the vasopressin function curve to the left. NaLoad elevated plasma [Na+] by 4.5% and vasopressin by threefold, but MAP and plasma ANP remained unchanged. NaLoad decreased PRC by ∼30%, ANG II by ∼40%, and aldosterone by ∼60%, regardless of diet and metoprolol. The natriuretic response to NaLoad was augmented during metoprolol regardless of diet. In conclusion, PRC depended on dietary sodium and β1-adrenergic control as expected; however, the acute sodium-driven decrease in PRC at constant MAP and GFR was unaffected by β1-receptor blockade demonstrating that renin may be regulated without changes in MAP, GFR, or β1-mediated effects of norepinephrine. Low-sodium diet augments vasopressin secretion, whereas ANP secretion is reduced.
- blood pressure
- sodium balance
- angiotensin
- aldosterone
- vasopressin
- atrial natriuretic peptide
the homeostatic regulation of renal sodium excretion remains enigmatic. It is generally accepted that the antinatriuretic actions of the renin-angiotensin-aldosterone system (RAAS) under most conditions dominate the regulation of total body sodium (8, 11, 26), whereas the antidiuretic action of vasopressin is crucial for the maintenance of osmolality (5). Together, these mechanisms provide the relatively independent control of renal sodium and water excretion rates indispensable for body fluid control.
Adjustment of renin secretion to changes in sodium balance is mediated by at least three mechanisms: renal baroreceptor activity, renal nerve activity, and the macula densa (MD) pathway (32, 41). The renal baroreceptor mechanism modulates renin secretion in response to the changes in renal arterial pressure (33, 35, 36). Renal nerves are mainly efferent renal sympathetic fibers providing sympathetic tone to multiple renal structures, including the renin-secreting juxtaglomerular cells (9, 10, 16); renin secretion from these cells is mediated by the action on β1-receptors of norepinephrine released from renal sympathetic nerve terminals as a result of renal nerve activity (hereafter called β1-mediated renal nerve activity). The MD signaling adjusts renin secretion (34) and afferent arteriolar resistance (29) to tubular ion concentrations. In the intact animal, renal arterial pressure and sympathetic nerve activity are easily related to body fluid volume. The relationship between fluid balance and the concentrations of sodium and chloride at the MD is less clear. In any case, uncertainty prevails with regard to the relative importance of the three pathways in the daily changes in renin secretion.
Studies of the effects of slow sodium loading of dogs and humans have indicated that robust natriuresis may be initiated without any increase in arterial blood pressure (1–4, 25, 27, 28). Actually, in one of these studies, the natriuretic response to acute sodium loading developed concomitant with a small fall in mean arterial pressure (MAP) (2), clearly illustrating that an increase in blood pressure is not a prerequisite for natriuresis. In these studies, natriuresis during sodium loading occurred concomitant with decreases in renin system activity, and deactivation of the RAAS seems to be a necessary condition of the development of a natriuretic response. This is supported by the results of another study in which plasma ANG II levels were clamped (by converting enzyme inhibition and infusion of ANG II) at physiological levels during sodium loading; the natriuresis was virtually absent as long as ANG II was administered despite the use of larger amounts of saline, which elevated the arterial blood pressure (7). Therefore, these results show that the natriuretic effect of small increases in blood pressure is easily overridden by the antinatriuretic effect of normal levels of activity of the RAAS.
Although it is possible that sodium excretion will be affected by undetectable changes in blood pressure and glomerular filtration rate (GFR), it remains remarkable that multifold changes in sodium excretion occur without any trend toward increases in either variable. Under such conditions renal nerve activity seemed to be the most likely mechanism controlling renin secretion and RAAS-dependent sodium excretion, i.e., slow sodium loading was assumed to decrease renal nerve traffic followed by a fall in the rate of secretion of renin and increase in the rate of RAAS-dependent excretion of sodium. Consequently, it was hypothesized that blockade of the adrenergic receptors mediating the secretion of renin would eliminate, or at least blunt, the deactivation of renin secretion as well as the RAAS-dependent increase in sodium excretion occurring during slow sodium loading.
The specific aim of this study was to investigate the response to a modest amount of sodium chloride without unnecessary volume signals. Therefore, the protocol included a very slow infusion of hypertonic sodium chloride simulating the intake of excess NaCl. However, this procedure stimulates the secretion of vasopressin, and it could be anticipated that changes in urine flow would render the measurements of renal clearances inaccurate. Therefore, the antidiuretic action of vasopressin was blocked by pretreatment with a vasopressin V2 receptor antagonist. Administration of vasopressin V2 antagonists to conscious dogs is associated with a robust positive clearance of free water (15), which unopposed would lead to dehydration. Therefore, body fluid volume was accurately sustained by means of a computerized servosystem controlling an infusion of sodium-free solution at a rate continuously adjusted to the urine flow. In this manner, deviations in total body fluid volume were kept within narrow limits (∼0.1%) throughout the experiments.
The experiments were performed in seven trained, conscious, beagle bitches weighing 13–16 kg. The dogs were kept in a group and fed either a commercial maintenance diet (daily intake of Na+/K+: 2.3/2.9 mmol·kg−1·day−1) or a custom-made very low-sodium diet composed of organic, salt-free peanut butter, organic oat flakes, and boiled rice. The sodium ion content of this diet was 0.003% and provided dietary intakes of sodium and potassium of 0.03 and 2.9 mmol·kg−1·day−1, respectively. The custom-made diet was provided for 7 days before each experiment. Prior to the study, the dogs underwent two-stage surgery during general anesthesia under antiseptic conditions as previously described (42). First, both common carotid arteries were displaced to skin loops to facilitate arterial puncture and a chronic episiotomy was established to ease the catheterization of the bladder. Second, bilateral ovariectomy and a hysterectomy were carried out to prevent spontaneous changes in sex hormone concentrations to affect the experiments. After full recovery, the dogs were investigated 18–20 h after the latest meal and 8 h after water withdrawal. The experimental protocol was approved by the Danish Animal Experiments Expectorate.
Experimental protocols.
On the night before the experiments, the supply of drinking water was interrupted at midnight by a timer-controlled electric valve to ensure a uniform degree of hydration in the morning. Baseline conditions, therefore, are characterized by some 9 h of water deprivation. In the laboratory, the dogs were placed in a sling and instrumented by sterile intra-arterial, intravenous, and bladder catheters allowing blood pressure measurements, intravenous infusions, and urine sampling, respectively. Arterial blood pressure and heart rate were measured continuously by computer based on 100-Hz sampling as described previously (19). Blood samples were obtained via the arterial catheter.
GFR was determined by the clearance of exogenous creatinine using bolus injection and continuous infusion as previously described (19); in the dog, values of creatinine and inulin clearances are indistinguishable.
In all experiments, vasopressin V2 receptors were blocked by bolus injection followed by continuous infusion throughout the experiments of the V2 antagonist OPC 31260 [1 mg/(kg body wt) plus 1 mg·(kg body wt)−1·h−1]. Regardless of urine flow, body fluid volume was maintained by servocontrolled fluid infusion based on continuous measurement of the body weight of the dog; a computer-controlled infusion pump kept body weight within ∼0.1% of the control value measured at the time of instrumentation.
After appropriate control measurements over 40 min, slow sodium loading was performed by intravenous infusion of 2 M NaCl solution at 10 μl·(kg body wt)−1·min−1 for 180 min providing a total of 3.6 mmol·kg body wt−1· experiment−1.
For any one dog, experiments were conducted with intervals of no less than 2 wk. The sequence of experiments was varied between the dogs. In part of the experiments, metoprolol was used for blockade of β1-adrenergic receptors [bolus 2 mg/(kg body wt), infusion rate 0.9 mg·(kg body wt)−1·h−1]. Metoprolol administration was started 60 min before the start of the control period and continued throughout the experiments (Fig. 1). It has been shown in dogs that similar regimens of metoprolol administration (0.5–2.0 mg/kg iv or 0.5–2.0 μg·kg−1·min−1 into the renal artery) abolishes the increase in renin secretion associated with low level renal nerve stimulation (17, 20), administration of the β1-adrenoceptor agonist prenalterol (21), and exercise (43).
Arterial blood samples were obtained and centrifuged immediately at 4°C. Analyses of sodium, potassium, osmolality, and creatinine in plasma and urine, as well as plasma concentrations of ANG II, renin (PRC), aldosterone, vasopressin, and atrial natriuretic peptide (ANP) were performed as previously described (19).
Data are reported as means ± SE. The results were assessed by one-way ANOVA adjusted for repeated measurements. In case of significance, all differences were evaluated by the Newman-Keuls test. Differences between series were tested by one-way ANOVA at the time of control or the time of peak deviation followed by the Newman-Keuls test when appropriate. Level of significance was P = 0.05. In cases of obvious inhomogeneity of variances, e.g., the results of sodium excretion, analyses were performed after logarithmic transformation.
On regular diet and no pretreatment, MAP averaged 112 ± 3 mmHg and heart rate was 60 ± 4 beats/min (Fig. 2). Both low-salt diet per se and acute metoprolol treatment during regular salt intake tended to decrease MAP (to 105 ± 4 and 107 ± 4 mmHg, respectively), but not to statistically significant degrees. Heart rate did not change with low-salt diet (62 ± 3 beats/min) or with metoprolol during regular salt diet (64 ± 3 beats/min). During low-salt diet, metoprolol treatment was associated with similar nonsignificant trends (MAP: 105 ± 4 to 101 ± 2 mmHg, heart rate: 62 ± 3 to 58 ± 2 beats/min). Values of plasma osmolality were 1–1.5% lower during low-salt diet compared with during regular diet (Table 1). PRC, ANG II, and aldosterone increased significantly during low-salt diet (16 ± 2 to 25 ± 4 mIU/l, 16 ± 2 to 31 ± 4 pg/ml, and 230 ± 26 to 1,750 ± 210 pg/ml, respectively, Fig. 3). Metoprolol treatment decreased PRC both on regular diet (−35%, P < 0.005) and on low-salt diet (−43%, P < 0.001), see Fig. 3. These differences in hormone concentrations were not associated with differences between the control rates of excretion of sodium, which across the series of experiments showed statistically indistinguishable mean values ranging from 0.7 to 1.9 μmol/min. Metoprolol pretreatment increased the basal rate of potassium excretion by threefold compared with nonpretreated conditions.
These data indicate that in the control condition prior to the acute salt loading, metoprolol-sensitive components of sympathetic tone, regardless of diet, controlled one-third to one-half of the renin system activity and was markedly antikaliuretic, but had little, if any, effect on blood pressure or heart rate.
Sodium loading, regular diet.
The sodium loading elevated plasma Na+ and osmolality by 4.5% over 3 h (Table 1) without change in MAP (Fig. 2) or plasma ANP (Table 2). The renin system variables (PRC, ANG II, and aldosterone) did not change during the first hour of infusion (providing 1.2 mmol NaCl/kg body wt); thereafter, progressive declines were evident (Fig. 3), and PRC, plasma ANG II, and aldosterone ultimately decreased by 30%, 39%, and 51%, respectively, compared with control levels. GFR was stable for the first hour of infusion, tended to become elevated during the second hour of infusion, and ultimately increased by some 12% (Fig. 2). Urine flow doubled and urine osmolality fell by 30%. In the individual dogs, control urinary sodium and potassium concentration ranges were 0.3–1.6 mol/l and 0.2–3.0 mmol/l, respectively. Urine osmolality varied between 86 and 127 mOsm/kg. Therefore, sodium and potassium salts together constituted < 10% of the urinary osmolytes. Sodium excretion increased markedly (8-fold, P < 0.0001, Fig. 2), albeit with large individual variations. In all but one dog, sodium excretion was clearly augmented, and in three of the seven dogs, the increase exceeded one order of magnitude. Potassium excretion increased more consistently, on average to about fourfold that of control (Fig. 2).
Sodium loading, low-salt diet.
As the result of the low-salt diet, control values of PRC, ANG II, and aldosterone increased by 53%, 93%, and 660%, respectively. In this setting, the salt-loading procedure increased plasma sodium, osmolality, and vasopressin concentration to levels very similar to those measured under normal dietary conditions. As expected, the renin system, activated by the low-salt diet, was inhibited by the sodium loading procedure, but remarkably, the relative decreases of the elevated PRC, ANG II, and aldosterone of −33%, −39%, and −55%, respectively, were virtually identical to the corresponding changes during the regular diet of −30%, −39%, and −51%, respectively (Fig. 4). The responses of plasma aldosterone are particularly illustrative; the 51% fall under normal diet (239 to 116 pg/ml) is in relative terms almost identical to the 55% decrease during low-salt diet (1,806 to 819 pg/ml), despite the seven- to eightfold difference between the starting points. GFR did not change significantly (Fig. 2). Urine flow increased by 86%, and mean urine osmolality decreased from 101 to 72 mOsm/kg; both changes are very similar to the corresponding changes during normal diet (87% and 105 to 78 mOsm/kg). Sodium excretion did not change significantly within the 3 h of observation (4 dogs showed very stable or slightly decreasing values, in 2 dogs modest increases were found, and 1 dog reacted with a steep 18-fold rise). However, potassium excretion increased sevenfold (Fig. 2).
During the low-salt diet, the renin system was deactivated by the standard sodium load to an extent, which in relative terms was very similar to the deactivation under normal conditions, but this was not sufficient to elicit a consistent natriuretic response.
Salt loading, β1-adrenergic blockade.
The metoprolol pretreatment altered control conditions as well as the response to sodium loading. The effects of metoprolol on the control conditions are described above. The standard sodium loading generated the same changes in plasma sodium, osmolality, and no changes in MAP or heart rate. The mean values of MAP at the end of the infusion was numerically, albeit not statistically, lower than the control values before the infusion, so not even a trend toward an increase in MAP was present. Under the acute metoprolol treatment, the renin system activity was decreased by sodium loading under both dietary conditions (Fig. 3). It is quite remarkable that 1) the sodium loading during metoprolol blockade markedly decreased PRC (−26% and −33%, regular and low-salt diet, respectively) and plasma aldosterone (−69% and −65%), and 2) that these decreases were very similar to those seen without metoprolol in PRC (−30% and −33%) as well as in aldosterone (−51% and −54%). GFR did not change at all during the sodium loading procedure; under normal diet the control GFR was 28.5 ± 2.9 ml/min and in the last 20-min period, GFR was 30.0 ± 2.4 ml/min (Fig. 2). As plasma sodium concentrations increased, the filtered load of sodium increased during salt loading (data not shown).
Under normal diet, the natriuretic response to sodium loading during metoprolol administration was robust (Fig. 2); one dog doubled the rate of excretion of sodium, the other six showed increases by more than one order of magnitude, on average showing a 24-fold increase (1.7 to a maximum of 41 μmol/min, Fig. 2). Under low-salt diet, the absolute values were lower (0.7 to a maximum of 15.9 μmol/min), and the individual responses were less consistent, but the average relative increase (22-fold) was very similar. Therefore, during β1-adrenergic blockade, sodium loading caused natriuresis independent of dietary regimen.
Measurable changes in blood pressure and GFR, and the presence of β1-mediated effects of norepinephrine do not seem to be necessary conditions for the hour-to-hour regulation of renin secretion. Furthermore, metoprolol pretreatment augmented the natriuretic response to slow sodium loading regardless of the dietary conditions.
Plasma vasopressin measured 1.6 ± 0.2 pg/ml and was not altered significantly by diet (1.7 ± 0.1 pg/ml) or by metoprolol (1.7 ± 0.1 and 2.2 ± 0.7 pg/ml). The salt loading procedure almost tripled plasma vasopressin (1.6 to 4.4 pg/ml, Table 2). This reflects the sensitivity of the osmotic control of the vasopressin secretion, and this parameter was not dependent on diet or metoprolol. However, values of plasma osmolality consistently were 1–1.5% lower during low-salt diet compared with during regular diet; therefore, the low-salt diet induced a leftward displacement of 4–5 mOsm/kg in the plasma osmolality to vasopressin function curve (Fig. 5).
The control concentration of ANP in plasma (Table 2) was reduced by some 30% during low-sodium diet (91 ± 9 vs. 129 ± 12 pg/ml, P < 0.001). Administration of metoprolol increased plasma ANP both during regular diet (129 ± 12 to 176 ± 25 pg/ml, P < 0.05) and during the low-salt period (91 ± 9 to 132 ± 12 pg/ml, P < 0.01). The effects of low-salt diet and metoprolol seem to be of similar magnitude because metoprolol treatment returned the value of the low-salt diet (91 ± 9 pg/ml) to a level (132 ± 12 pg/ml) indistinguishable from the normal control (129 ± 12 pg/ml). In contrast to these changes with diet and metoprolol, the sodium loading procedures did not produce any change in the concentration of plasma ANP, except for a transient increase 2 h into the salt-loading procedure in one of the series (metoprolol treatment during low-salt diet); despite continued sodium loading, plasma ANP returned to control values.
Our results show that although the administration of metoprolol reduced the circulating levels of renin substantially, it did not impede the deactivation of the renin secretion or the natriuretic responses to salt loading. The present study was designed to show that the renal nerves play a key role in the regulation of total body sodium under physiological conditions. We hypothesized that blockade of the adrenergic receptors mediating the secretion of renin would eliminate, or at least blunt the deactivation of the renin system occurring in response to modest salt load and that this reduced reactivity of the renin system would impede the acute natriuretic response to the salt loading. The results are incompatible with the hypothesis. Adrenergic β1-blockade (preventing the transmitter as well as the circulating hormone function of norepinephrine) does not prevent acute regulatory downregulation of renin secretion, at least not in relative terms, and augments the renal excretory response. Clearly, a change in arterial blood pressure is also unnecessary for the deactivation of the renin system and the corrective natriuresis associated with salt loading. Increases in GFR were absent during three of the four loading procedures. Together, the results unexpectedly demonstrate that the primary homeostatic control of the renin secretion, and thus the RAAS-dependent sodium homeostasis and blood pressure control, is not coupled directly to arterial blood pressure, GFR, or β1-mediated effects of norepinephrine.
In several respects, the present data are analogous to recent results obtained in mice deficient in β1- and β2-adrenergic receptors (18). They showed that chronic absence of these receptors caused marked reductions in PRC but also that the responses to a number of acute and chronic inputs to renin secretion persisted albeit at reduced magnitude. In particular, the PRC responses to high- and low-sodium diets were well maintained in these double knockout mice. However, the study did not address the mechanisms involved in the changes in PRC caused by alterations in sodium intake in the absence of the β-adrenergic receptors.
Even if the homeostatic regulation of renin secretion may take place without changes in arterial blood pressure, GFR, and β1-mediated effects of norepinephrine, several mechanisms may be responsible for the change in renin secretion. A direct effect on osmolality on juxtaglomerular cells is a possibility; other mechanisms include 1) concentration signals operating via MD, 2) a component of renal sympathetic nerve activity not mediated by β1-adrenoreceptors conveying signals form the central nervous system, or 3) an extrarenal humoral substance provided to the kidneys by the blood.
It is well known that the secretion of renin from juxtaglomerular cells in vitro is sensitive to extracellular osmolality (12, 37); it was shown that small elevations in osmolality clearly decreased renin secretion and vice versa, and it was hypothesized that this mechanism could be operative in vivo (12). Recently, it has been reported that in single mouse juxtaglomerular cells, lowering of bath osmolality by some 3% increases cell capacitance (by whole cell patch clamp), indicative of exocytosis, and augments renin release by 20-fold (38). However, the specific role of osmolality in the homeostatic regulation of renin secretion in the intact animal has been difficult to ascertain (6). Recent data from isolated, perfused kidneys seem at odds with the mentioned in vitro results even with regard to the direction of change. In the perfused kidney model, renin secretion consistently was found to be stimulated by an increase in plasma osmolality (22). The present results in the conscious dog do not necessarily express a direct, causal relationship between plasma osmolality and renin secretion; but if this were the case, they support the notion of an inverse relationship (12) between plasma osmolality and PRC.
In addition to a direct effect, it is also possible that under the present conditions, the acute sodium loading caused subtle changes in GFR as well as in proximal and loop-of-Henle reabsorption rates so that tubular fluid composition at the MD reflected the level of total body sodium. Although GFR did not change, the filtered load of sodium increased because of the increase in plasma sodium concentration. The concentration of NaCl at the MD is a complex function of GFR, filtered load of sodium, glomerulotubular balance, tubuloglomerular feedback, and the regulatory control of proximal reabsorption (39); the authors estimated that roughly one-half of a 10% increase in the filtered load of sodium would arrive at the MD. Extrapolating the estimates of Thomson and Blantz (39), the author be assumed that the increase in solute concentration at the MD could be substantial (up to 75 mmol/l) depending on the degree of increase in tubular flow rate, and that the increase would be minimal only at unrealistically high increases in tubular flow. It is, therefore, a definite possibility that augmented sodium reabsorption by glomerulotubular balance and/or MD mechanisms lead to deactivation of the RAAS. Several hypotheses seem justified with regard to the coupling to juxtaglomerular cell function. It could be speculated that increases in interstitial concentrations of adenosine, elevated by increases in tubular transport and operating via A1-receptors, reduce renin secretion, ANG II concentration, and aldosterone production, leading to increased sodium excretion, (cf. 40). Small or immeasurable changes in GFR and minor deviations in tubular function could play a major role in the present deactivation of the renin system in response to salt loading. If so, the regulation of total body sodium relies heavily on the complex interaction between renal vascular and proximal tubular functions including glomerulotubular balance and tubuloglomerular feedback.
Up to a few years ago, it was widely believed that the renal nerves were the crucial link between baroreceptor activity to alterations in the renal excretory functions serving blood pressure control (24). Recent evidence seems to have questioned this concept because it was demonstrated that the presence of the renal nerves is not a necessary requirement for achieving long-term changes in arterial pressure during prolonged baroreflex activation (23). The present experiments were not designed to exclude the possibility that fractions of renal sympathetic nerve activity, other than that mediated by β1-receptors, may be involved in sodium reabsorption, and therefore, in the control of total body sodium. In this context, it should be noted that the effects of systemic β1-adrenergic blockade in the intact animal may be complex. Results of renal nerve recording in anesthetized rabbits before and after administration of the atenolol and propranolol have been interpreted to indicate that these cause a reduction in renal efferent nerve traffic (13, 14) concomitant with the expected decrease in arterial blood pressure. The effect on renal nerve activity was believed to be associated with an (unexplained) increase in arterial baroreceptor activity (14). If these results, despite some internal inconsistency, represent a general phenomenon, it can be assumed that in the present experiments metoprolol administration decreased efferent renal nerve activity. We administered metoprolol well in advance of the salt-loading procedure, and the β1-adrenergic blockade caused no significant change in any of the measured values except potassium excretion, which was significantly elevated by metoprolol. Any direct inhibitory effect of metoprolol on efferent renal nerve activity seems to have had little effect on renal excretion of sodium and water, but may still have decreased the nervous input to functional renal adrenoreceptors, i.e., receptors other than β1. So, in addition to the decrease in renin secretion, metoprolol may have changed the setting in which the renal response to salt loading was expressed by decreasing sympathetic tone to the kidney.
Afferent and efferent nervous pathways are most likely operative under the present conditions. The central nervous system is able to respond to very small changes in plasma sodium concentrations. Infusion of hypertonic saline to conscious dogs in amounts so small that they did not produce measurable changes in plasma sodium or osmolality were nevertheless associated with marked changes in plasma vasopressin concentrations (27), emphasizing the exquisite sensitivity of the osmoreceptor. It is, therefore, highly likely that the present perturbation generated abundant afferent input to/in the central nervous system. With regard to efferent mechanisms, it was concluded a few years ago that available results prove that renal tubular effects of low-frequency renal nerve stimulation are mediated by α1-adrenoceptors located at the basolateral section of the renal tubules and are functionally important under certain circumstances (9). However, although present and potentially significant, little is known about the homeostatic importance of these elements of renal nerve activity under normal physiological conditions.
Extrarenal natriuretic substances may play a key role on the regulation of total body sodium taking place at constant blood pressure. In the present experiment, we measured the ANP concentrations. Plasma ANP decreased during the low-salt intake and increased in response to the β1-receptor blockade. These responses are not surprising, but the present experiments were not designed to elucidate the mechanisms involved, e.g., atrial transmural pressures were not measured. The effect of acute sodium loading on plasma ANP was minimal. With the exception of a single, small (30%) increase in plasma ANP occurring transiently after 2 h of salt loading under low-sodium diet and β1-blockade, plasma ANP was not affected by the sodium loading. Therefore, circulating ANP cannot play a major role under the present conditions. Other circulating substances may be involved. The possible regulatory functions of adrenal cardiotonic steroids, such as ouabain and marinobufagenin, have been reviewed recently (31). However, although the latter, in particular, has been associated with sodium metabolism under experimental conditions, both the regulation of the release of these substances and their specific effects on renal function appear unclear (30, 31). The evidence demonstrating a causal relationship between circulating levels of any of these substances and the homeostatic control of total body sodium under physiological conditions does not appear persuasive.
Numerous other modulators of renal function may be involved in sodium homeostasis, e.g., prostanoids, nitric oxide, bradykinin, endothelin-1, and dopamine. Common to all these substances is that they have been shown to be able to affect renal electrolyte excretion, but also that none has been shown to be a mediator, i.e., a plausible working hypothesis linking the natriuretic/antinatriuretic effect of the modulator to sodium intake or total body sodium does not exist.
In summary, the relative decrease in renin secretion in response to acute salt loading is unaffected by metoprolol; therefore, β1-mediated adrenergic control does not mediate the acute, regulatory inhibition of renin secretion, although it does codetermine the level of PRC. The present increase in plasma osmolality of 4–5% may have mediated a decrease in renin secretion; however, the specific nature of this powerful controller of renin secretion remains to be identified.
The present model of highly trained conscious dogs represents the sedate conditions of resting mammals. In contrast to renin secretion, heart rate and blood pressure were low and insensitive to metoprolol, indicating a very low sympathetic drive to the circulation and homeostatically relevant sympathetic tone to the juxtaglomerular cells. In this setting, renin secretion was dependent on factors other than arterial blood pressure, GFR, and β1-mediated effects of norepinephrine. This finding opens the possibility that the primary mechanism of sodium homeostasis is either an intrarenal mechanism or an extrarenal blood-borne "natriuretic" agent. There is no shortage of intrarenal modulators of renin secretion (e.g., adenosine), nor of potential natriuretic agents (e.g., cardiac glycosides), but it is difficult to see which candidate could qualify as the homeostatic mediator of sodium metabolism.
The interaction between the central nervous system and the kidney is crucial for understanding the mechanisms behind major pathologies such as hypertension. However, without a clear picture of the normal homeostasis, the foundation for clinical hypotheses remains unreliable.
The work was supported by the Danish Medical Research Council and the NOVO Foundation.
The expert technical assistance of Bodil Aarup Kristensen, Ulla Melchior Hansen, and Ole Madsen is gratefully appreciated.
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 © 2009 the American Physiological Society


text:
MURS Alert Transmitter
Average Customer Rating(1 ratings)
Featured Customer ReviewInstrumental in catching 3 thieves in the early morning after unit installed six months earlier. [ read more ]By Owners from North Augusta SC
Dakota Alert MURS Alert Transmitter
- Offers the ability to monitor activity at remote locations
- Capable of sending 4 different alert messages to the transceiver
- Will give you real time monitoring of remote locations up to several miles away
Product Overview
Dakota Alert MURS Alert Transmitter
MURS Alert Transmitter
The MURS Alert Transmitter offers the ability to monitor activity at remote locations by utilizing passive infrared sensor technology that will send an alert signal to the MURS transceivers in order to notify you that someone has entered a monitored area. Alert signals will be in spoken English and are easily selected at the transmitter so that separate zones can be monitored at the same time and will give you real time monitoring of remote locations up to several miles away. There are many different applications; it can be used by security guards, small businesses and also by hunters monitoring game trails; any scenario that requires immediate notification when someone or something enters a monitored location. Authorized by the FCC, MURS (Multi-Use Radio Service) is a license free service that allows the user to transmit voice and data. MURS also allows a maximum of 2 watts of output power; which means greater range than other license free radio services. Length: 7 1/2"/ Width: 6"/ Height: 4.6"
Place Your Order Here
Dakota Alert MURS Alert Transmitter
MURS Alert Transmitter Reviews Summary
You have already voted for this. Thank you
You cannot vote for your own question or answer. Thank you
MURS Alert Transmitter
Ask the community about this product and get answers. Share your knowledge and advice. Learn More about Q&A.
0 Questions | 0 Answers
Part Number(s): 141 0303
Mfg Part Number(s): DK-MAT
Scrip Part Number(s): 141 0303
Because our price on this item is lower than the manufacturer's suggested retail price, the manufacturer does not allow us to show you our price until you place the item in your shopping cart. Retailers like Allegro Medical have the legal right to sell products at prices we set. However, adding the item to your cart allows us to show you our lower price consistent with our promise of always offering you the lowest possible prices on the widest selection of medical supplies, medical equipment and life enhancing products.
Adding this item to your shopping cart won't require you to buy it. However, our prices do change. If you decide to purchase this item now you are guaranteed the price now displayed in your shopping cart. Complete your purchase by clicking on the "checkout" button or simply remove the product from your cart if you decide not to make your purchase at this time.

subset: commoncrawl


text:
Backpacking Big Sur: Sykes Hot Springs
posted in: ADVENTURE, Blog, California, Hike, TRAVEL, United States | 0
Where: Big Sur, California. Sykes Hot Springs Best Time To Go: Spring, early Summer.. It get's super hot on the trail when the trees are scarce. Length of Trip: 20 miles. You could do it in a day if you're … Continued


text:
Larue – Personal Blog
Larue is a modern & stylish blog template, that can give your readers a immersive browsing experience. Larue polished & beautifully balanced pages make it an ideal template for almost all types of blog.
If you interested in BUYING ALL RIGHTS, you can book our next PSD – contact via email: [email protected]
- Polished inner pages
- Three Exquisite Home Pages
- Professional Post Formats
- Balanced Grid System
- Easy to Customize
- Eye-catching Typography
- Free Google Web Fonts
- Raleway
- PT Sans
- Shutterstock
- All Images are not included


text:
Jexxx's Favorites
5 votes cast
2 votes cast
Jexxx has not updated their status recently.
No tags yet...
Only Jexxx's favorite artists and friends can post to this wall. You can add a post if you become friends with them.
Join Zivity now to join the conversation.
Thank you for voting for Erin Michelle in "Sunday Morning Girl"
You're welcome :)
Thanks again!
Hey there :)
Hello :)
How are you?
I'm good. How are you?
Pretty good, thanks
Pretty good, thanks
Welcome to Zivity! It's good to meet you. Have a great Wednesday! Hey, I am the very first to write on your wall.


text:
Science resources & picture books
Expand Messages
- It's STEM Friday - and that means science resources for kids & adults who love to investigate science with children.I was fooled by a couple days of sun and thought that leaves - or at the very least our forsythia - would be breaking bud by now. Ha! The blue jays and juncos were hiding in the snow-covered branches yesterday.Still - if and when spring ever comes, I've got some hands-on leaf activities at Archimedes Notebook (http://archimedesnotebook.blogspot.com/2013/03/leaf-watching.html)And over at Sally's Bookshelf I've posted a review of "First Dog Fala" - another presidential bio through the eyes of a first pet. But there's more: links to cool resources on presidential pups and a game, plus it's Perfect Picture Book Friday which means links to lots of cool picture book reviews. (http://sallysbookshelf.blogspot.com/2013/03/first-dog-fala.html)Hope this helps fills the homeschool wish-list for stuff to do on yet another "where did spring go" upstate NY day....~Sue
- If you're looking for a book that encourages girls to explore engineering - check out Rosie Revere, Engineer at the STEM Friday blogOver at my Archimedes Notebook blog you'll find some resources for kids to explore engineeringMeanwhile, I'm delving into biographical haiku with "Cool Melons Turn to Frogs" at Sally's BookshelfIt's part of Perfect Picture Book Fridays, which means you'll find lots of book-extending activitiesMake sure to drop by Susanna Hill's blog to find links to lots more picture books - and related activities.
Your message has been successfully submitted and would be delivered to recipients shortly.


text:
So … Who Wants to be a Millionaire? With the Coming Global Currency Reset, Just About Anyone Can…..If They Want to!!! Here's Some Practical Thoughts and Advice!
Steve Beckow has encouraged folks to purchase Vietnamese dong for the coming Currency Exchange (C/E). I hope I can add some information to help those who are not sure about getting involved or have some questions.
But first a little background on me. Many of you may remember me as the initial Director of The Hope Chest and the co-host on the "Let's Talk 2012 and Beyond" radio program, and just last week I started a new radio program on Wednesday nights called "The Sedona Connection."
But, I also have a background in banking and finance, was a former State Senator and have been a market trader for over 17 years.
Read More Link On Right
I now live in Sedona, AZ and I'm helping a group of about 50 of us that have purchased dinar and dong……we're all about to become overnight millionaires and we are taking the prudent steps of being responsible with our new gift of wealth.
I've been writing, giving help, direction and practical application to the group now for about 5 months, so here's extending it to a larger group with some practical Q&A.
Many of you have friends or family you'd like to have participate in this C/E but they are not about to believe in a channeled message from an angel or a simple statement from Steve. They want some proof or practical reasoning about what is about to happen. This Q&A should help.
What is the Global Currency Reset or Revaluation?
While the Iraqi dinar has had most of the attention, there's actually a complete global currency reset about to happen. About 198 currencies in the world are being reset backed by assets and commodities such as gold, silver, oil, wheat, rice, etc. Various economists and experts have said we must do this or the whole global financial system will collapse.
What is the Basis of This Currency Reset?
A few weeks back there was a You Tube video posted on the Golden Age of Gaia by Bix Weir mentioning the elimination of worldwide debt. The real basis of the interview was the coming currency collapse.
All of the G8 countries (U.S, Canada, France, Great Britain, Germany, Italy, Russia, and Japan) have fiat currencies, meaning there is nothing backing them up but the good faith of the government. We know how good that has been; most of them are bankrupt.
The Federal Reserve in the U.S. can print money at will and put it into circulation at any time. They've been doing this by the trillions for the last few years, it's obvious they think money can grow on trees as they can just print up whatever they want whenever they want.
This normally causes a huge cycle of inflation, devaluing of currencies, and leads to a collapse.
Every fiat currency in the history of the modern world has eventually collapsed and all of the G8 countries are currently in debt beyond their ability to recover.
They are all theoretically bankrupt beyond their ability to pay back their debt, meaning it's only a matter of time before their currencies collapse. This printing of trillions is just kicking the can of collapse down the road.
Bix stated we are on track for this collapse in the next 2 to 4 months. The collapsing currency also eliminates all debt as money has become worthless. He stated we are on a path of two choices, currency collapse or a global currency reset backed by commodity assets. One is inevitable (the collapse) if we do not do the other (the reset).
Who's Behind this Currency Reset?
The shadow governments controlled by the cabal/illuminati have manipulated the global finances of the modern world for a couple of centuries. They currently manipulate and control the stock market, price of gold and price of oil.
They have deliberately kept about 60% of the world's population living on less than $2 per day and the rest of the developed world in some form of economic slavery. The ultra-wealthy 1% has controlled the rest of the world's population through the power of controlling the world's money supply.
Their lust for power and control is about to all fall apart. A coalition of about 160 countries led by the BRICS nations (Brazil, Russia, India, China, South Africa) have formed a united front on the G8 and called their bluff of corruption and greed.
The G8 so weakened the world economy that it gave way for the 160-nation coalition to step up and call "check" in the world financial chess match. It's game over; the coalition is demanding a return to asset-backed currencies to stabilize the world economy.
The IMF (International Monetary Fund), World Bank and BIS (Bank of International Settlements) have quietly been working on this reset for 5 to 10 years.
Why are the Iraqi Dinar and Vietnamese Dong so Important?
There are three currencies that are way out of balance with the rest of the world; the Indonesian Rupiah is the third. While I'm not familiar with Vietnam's full story, Iraq's has been more center stage.
Both of their currencies were devastated from their wars with the U.S. as their currencies can be purchased for 1/10th of pennies on the dollar. In 1990 when Saddam Hussein invaded Kuwait, the country was placed on economic sanctions by the U.N.
They could not trade their goods on the open international market and their currency was taken off the foreign exchange. This is what is meant by U.N. Chapter 7 seven On June 27th, the U.N. Security Council voted 15-0 to remove Iraq from chapter 7 and return them to chapter 6 status.
They once again became a member of the international trading alliance, but to do so they must bring their currency back onto the foreign exchange market, meaning it must be revalued.
Today 1162 dinar will trade for $1 U.S. In 1990 before the sanctions .29 dinar would trade for $1. To reverse the trade value, in 1990, 1 dinar would trade for $3.47.
Today approximately 21,100 Vietnamese dong will trade for $1 U.S. So you can see the huge imbalance. When the currency reset is backed by commodity assets those values will skyrocket and come back into balance with the rest of the world.
So Why Are the Dinar and Dong Going to be So Valuable?
Each country's currency value will be based on the country's tradable commodity assets. Not only does Iraq have the 2nd largest oil reserves in the world, but they have huge gold mines. Many are speculating that Iraq's dinar could become the strongest currency in the world.
Their Prime Minister was recently quoted as saying, "We have billions and billions barrels of oil to trade, but we do not even have running water." Their country has been devastated by war and they want to rebuild. They are hungry and anxious for this reset to happen and are willing to pay handsomely for it.
For Vietnam, it's rice, the world's largest food commodity. Vietnam is the 2nd largest rice producer in the world and they have offshore oil rigs.
They have been selling their rice and oil to China who has kept their currency in suppression since the war. Based on an open and free market the value of their rice and oil will explode to be on par with the rest of the world.
So, What are the Exchange Rates of the Dinar and Dong going to be?
That's the trillion dollar question!!! Some individuals have been working on this C/E for close to 10 years. For most of that time speculation had the dinar returning to its 1990 value of $3.47 and the dong around $.47. Based on talking with scores of people involved and reading the blog sites every day, I believe these are the minimum rates.
But, in the last month so much has changed. The key was the U.N. vote on June 27th to bring Iraq back into the global open market, when that happened everything changed.
Since then the blog sites have been saying the reval could happen any day now. But, things do seem to change every week, let alone almost every day.
What most people don't know is the U.S. government has trillions of dinars to exchange. They want the value to be high so they can pay off the U.S. debt and they have been negotiating behind the scenes to get the rate as high as possible.
Many insiders who have contacts in the IMF, U.S. Treasury, the Central Bank of Iraq, and some of the larger banks in the U.S. have been reporting the rates are already appearing on the back screens of the bank officers' computers.
This has been going on for over a month and the rates are reported to be very very high. While this is all speculation at this time, the intel appears to be reliable.
Some feel those rates are just test rates and will not be accurate, while others are reporting those are the C/E rates for the private groups (I'll explain that later.)
OK, OK…. So what are the Exchange Rates?
Speculation has the minimum rates of the dinar at $3.47 and the dong at $.47. The upper rates… I hope you're sitting down … The dinar is at $23.50 and the dong at $3.60. Do the math; you'll see why we can get excited!!!
100,000 dinar minimally will become $347,000 and 100,000 dong will become $47,000. At the high end 100,000 dinar will trade for $2,350,000 and 100,000 dong will become $360,000.
So……What are the Costs?
There are different options for purchasing the currencies. Because the dong is currently tradeable it can be purchased at a local bank. But, don't expect to walk in and get the currency the same day.
Most of the banks have to order it from larger HQ's and it will take about 3 days before you will have it in hand.
As Steve mentioned, you can also go to a foreign exchange at a local airport. But, I wouldn't count on that either. For security reasons they don't keep large quantities on hand.
The larger quantities you would likely have to get through a bank or through the online certified dealers.
You can purchase 100,000 dong for about $12-$14 at a bank. You can get the same for about $18-20 online. Dinar or dong can be purchased by certified online dealers.
You can google them, but make sure they are certified and guarantee shipment. You can acquire 100,000 dinar for about $30-$40 online.
Those are total costs which include the currency, the transaction fee, shipping and handling and a small profit for the dealer/broker. Most of the online dealers require a money wire and extra for Fed Ex shipping.
There's one myself and our group of about 40 in Sedona have been using. We pay a few extra dollars per transaction, but we have all been very pleased with the level of service. One flat fee covers everything and we have the currency in hand in about three days from the time of order.
They are also one of the very few who allow you to use a debit or credit card and they also have a 7 day guaranteed return policy, no questions asked.
Do the Math!!!
Here's the bottom line, using the higher costs, $20 can buy you 100,000 dong that minimally turns into $47,000. $120 can buy you 100,000 dinar that minimally turns into $347,000. Rates vary based on volume purchased, but you get the idea!
So……What's the Real Bottom Line, in Other Words, What About Taxes?
That's another million dollar question. Tax implication is something we cannot overlook.
There are all kinds of speculation and rumors floating around on the blog sites regarding taxes. I've done my homework, but there is more to the story.
Before taxes, the dong is a better return on the dollar if the rates are higher across the board. But, reliable intel information is saying there may be a huge tax advantage in purchasing the dinar.
What is the Current Law Regarding Taxes?
I can only speak to U.S. law and do not have the time to do the hours of research for other countries. Rumors, rumors and more rumors are floating around about what the President or others are going to do about the taxes for the C/E.
My advice from someone who was a lawmaker (Senator) for 12 years; stick with the current law until you have solid proof otherwise. The U.S. Constitution is clear, only Congress can impose a tax.
The law does not allow a tax to be implied retroactively, so the current law applies until something else is passed through Congress.
The current law considers an increase of value in a currency an investment and is taxed as a capital gain. Period!!!
IRS Publication 525, page 30, "Taxable and Non Taxable Income, any increase over $200 is considered a capital gain. Here's the link to the publication to read it yourself: http://www.irs.gov/p...525.pdf#page30.
So, What is the Capital Gains Tax Rate in the U.S.?
There are two rates for capital gains, short term and long term. Long term is having the asset in possession for more than one year. If you purchased your dinar or dong more than one year before you exchange it, it will be long term.
Make sure to keep your receipts for your date of purchase. If you can't prove your date of purchase it could be very very costly.
Anything less than one year is short term. But here's the key, they date is not based on when the Reval takes place, but the day you exchange it. The capital gain is not considered a tax until it is realized, or turned in.
So What's the Rates?
Short term is taxed as normal income. Those rates vary based on the amount of your taxable income. The top U.S. rate for 2013 is making over $450,000, most of us will qualify for those rates
Short term top rate: 39.6%
Long term rate: 20.0%
Here's the scoop, most U.S. citizens should plan on paying 40% to 45% of their reval earnings in taxes. Don't forget your state taxes, those vary from state to state and are different based on capital gains state laws.
Why Could the Dinar be a Far Better Value After Taxes?
That's another million dollar question, but first, the rest of the story. When I was first approached about purchasing dinar, I asked …….who's going to pay the trillions of dollars for the increase in value of the RV. Answer…..China……how…..oil credits.
Iraq has billions of barrels of oil, China has billions of people and China has trillions of U.S. dollars from the decades of purchasing U.S. bonds. It cost Iraq $2 to produce a barrel of oil, while the current market is about $104 per barrel.
Iraq wants to have as many of the dinar, now in our possession, in their country quickly. Here's what's supposed to be coming down, but remember it is all speculation until proven otherwise.
China is willing to pay the higher rate for the dinar from us, paid for by their trillions of U.S. bonds. They purchase the dinar in a private exchange and then use those dinars to purchase oil from Iraq at $30 per barrel vs. the open market of $104.
This produces a win-win-win scenario. We win by the higher dinar exchange rate, China wins by receiving billions of barrels of oil at a discounted rate and Iraq wins by quickly receiving their dinar back so they can rebuild their country.
Here's the other tax implication, creating a great savings for us. This exchange could be considered a commodity exchange, not a capital gain and it could be considered tax free.
Yes, that means we may be able to receive the full exchange value with no tax implications. The jury is still out on that decision as it is one of those gray areas in current tax law.
In that situation the President has leeway to decide how it can apply and has supposedly brokered a deal with China. As of now, the speculated deal has China paying an 11% tax on the dinar/oil exchange and we will pay nothing. He also was the one who supposedly was able to get the dinar rate up to around $23.
The President wants the higher rate so the government's dinar can be used to pay off the U.S. debt. Also, U.S. is China's largest export partner. When millions of U.S. citizens have millions of new dollars to spend, China benefits from our purchasing their goods. It's another win-win-win proposal.
Because this tax deal applies to the oil credits, it appears to only apply to the dinar and not the dong. While some are saying the tax free exchange may apply to the dong, there is very little intel backing that up.
Based on the inside intel, if this happens the dinar is by far a better return after taxes.
As a straight up purchase, and applying the 39.6% tax rate, and using the minimum exchange rates, the dong is a better value on the dollar spent.
But, the intel for the dinar is far more positive and the potential for exchanging them tax free gives them a better odds. The dinar can revalue without a global currency exchange while the dong is dependent upon it taking place. There is far more reliable intel on the dinar than the dong.
So, what should we do?
I can't give you a direct answer, there is so much speculation on both sides and so many variables that we cannot accurately verify. But, here's what I did. I made a number of purchases over a few months.
Each time I would go into meditation and inquire from my higher self. I felt it was prudent to have dinar and dong, but leaned to the dong side. It depends on how much money you want to spend, what you can afford and what type of guidance you receive from within yourself.
How should I tell this to my friends?
There are two ways to look at this, the esoteric/metaphysical side with info from channeled angelic sources and the practical 3d world perspective.
I've tried to give you the more practical info so you can share this with friends and family who will not listen to a channeled angel source of info. In other words you can share this info with others without them thinking you're crazy.
There I so much more info available on the esoteric side that gets me so excited about the higher rate, but, space is limited for now.
What do we do When It's Time to Cash In?
There are reported to be three different exchange rates.
1. The street rate, what you get if you go to the bank teller window as an individual.
2. The ability to negotiate your own rate with a bank of your choice.
3. The private group rate.
What is the Private Group Rate Exchange?
It is reported the private group rate is going to be the best. In fact many are implying the street rate could be the lower $3.47 while the private rate may be as high as $23.50. But, this is still all speculation.
Why? The China oil credit issue. The currency you exchange at a bank will go directly to Iraq and not to China. The private group exchange goes directly to China and they use it to purchase the discounted oil.
How Will I be Notified of the Group Exchange?
Wells Fargo bank is working as the independent broker for the group. You must be on the email list. When the RV happens they will send out an email to the list giving an #800.
You will call that number, they will verify your email, you will give them your zip code and they will direct you to the closest private exchange center via you location. This will be a private exchange with Wells Fargo employees and will not be at a local bank branch for security reasons.
Do I have to Accept or Use Wells Fargo for this Exchange?
Nope, it's totally your choice based on the three options listed above. But, if you get my drift, you would be crazy to not consider it and at least check it out. Why?
You can take your dinar into a bank, receive the lower $3.47 and have to pay about 40% in taxes.
Or you can take your dinar to the private exchange, receive upwards to $23 and potentially pay no taxes…..DUHHHHH…..NO BRAINER……unless you like paying high taxes, throwing your money away and making the bankers get richer.
How? Those bankers who give you $3.47 are going to take that dinar and exchange it for the higher $23. They're not stupid; they're in the business of making money for their bank and bonuses for themselves!!!
When is this RV Going to Happen?
Any Day……Seriously…..it could be tomorrow! All the reports say it should have happened two to four weeks ago.
I have chosen to not give you any specific currency broker, etc. as I want to respect others choices. But, as stated all of us in our group of about 40 in Sedona have been very happy and comfortable with who we are using.
We've been having meetings in a private home to support each other, learn from each other, and give info to each other.
We're researching local CPA's, tax attorneys and financial planners to use after we receive our money.
One night I gave a presentation to a group of about 15 people in my home. We talked taxes and other ways to be prudent with our new wealth. We've formed a foundation as a 501©3 non-profit that we are going to use for funding community projects.
So, Who Wants to Be a Millionaire?
You're being given a once in a millennium opportunity to become an overnight millionaire!!!
What's the risk? $20-$40…..shoot, I waste that much on a bad bottle of wine or ... a poor choice of an evening dinner at a restaurant! So get with it!!!
Blessings!!! Dave Schmidt LINK
9/23/2013 10:33:46 am
Wow!! That was very thought provoking.
9/23/2013 10:47:06 am
I bought some Dinar and Dong thru an on line site and was very happy with the service. A very good friend who is much older does not use a computer and asked me if we could buy together. I ordered it all under my name, and she gave me cash to put in my checking account for her share. I received all the currency via fed ex and gave her share of Dinar and Dong to her. Is there going to be any type of problem when we go to do the currency exchange???? I have told her to put at least 50% away for taxes.
Dee Narr
9/23/2013 11:26:03 am
I did the same thing and had the person who ordered it make a copy of reciept showing date of purchase as well as a letter stating we went in on this together...
9/24/2013 03:26:54 am
Hi - I sold several friends and relatives a few dinar and gave them a receipt for it, we both signed the receipt so they could use that for the taxes. They paid me cash, and I put that on the receipt.
9/23/2013 10:58:50 am
Very well done. You summed things up nicely. Thank You Dave.
9/23/2013 11:22:43 am
Thank-You Dave! Much needed!!
9/23/2013 11:34:47 am
Ok, just a question about Russia...it states above they are part of the G8 AND BRICS? A little confused, sorry. Thanks for any clarification.
9/23/2013 01:20:15 pm
Russia is a par of both. They were added to the G8 a few years back and are a part of the BRICS. Don't ask me why, I just know they are.....thanks....Dave
Robert hollmann
9/23/2013 11:46:01 am
thank you so very much for this explanation. I have heard pieces of it but didn't quite understand the full implications. You did a great job
9/23/2013 11:51:05 am
Thank you for tying this together, assuming its accuracy, this is an important thing for all of us, and those we may be trying to explain our investment to. However, it does lapse into more of bit of a sales piece. I am happy to see all spiritual paths honored here.
9/23/2013 12:51:15 pm
Excellent Dave. Best explanation in 3 years for me. Where and how can you get on the Wells Fargo list and 800 calling?
9/24/2013 01:34:07 am
I agree with everybody, this post is excellent. And I have the same question as matala: How does one get on the list and thus the 800 number? Please provide this information, Dave! Thank you so much and thanks again for the amazing post.
9/23/2013 01:01:00 pm
How do I get on the email list for the wf 800#
9/23/2013 01:04:37 pm
thanks for all the information, and the opportunity to give us a positive change in our lives, all blessings to all.
9/23/2013 01:12:38 pm
I think that one of the few benefits of this delay - delay - delay roller coaster ride is that I will now get long term capital gains on my dong. It was money in the bank to wait -- about 20% less taxes.
9/23/2013 01:35:40 pm
David, Thank you so much for the wealth of information, so appreciate, look forward to more post!! Blessings!!
9/23/2013 01:36:15 pm
Thank you, Dave, for writing this so simply for us to share with others. Now I'll be able to educate my wife, whom I haven't told of the Dinar/Dong. You give me instant credibility.
9/23/2013 02:09:23 pm
Dave, you've done a great job of cogently and articulately putting so many of the pieces of this puzzle together. Since I began assimilating what was in the beginning scattered pieces of disparate information, as things have connected together, part by part, it has made increasingly plausible sense. Those who are naysayers, and have as their mantra, "It's NEVER happened before, and therefore it CAN'T happen now, and therefore WILL NEVER happen, are, in my opinion, making a costly error of intellectual arrogance. The fact is that the conditions which are present at this time have never presented themselves in this "matrix" before in history, and therefore people of intellectual open-mindedness, spiritual strength, and creative vision are able to understand that out of these unique conditions a tremendous opportunity for "the small people" to profit can arise. In the light of your article, and this may be my unique contribution to the community at this time as a matter of record, this is likely to be true in conclusion for the following simple clear reason and thought: At this moment in time, our own unique and personal financial interests may dovetail with and further the causes of much larger entities and concerns. In particular, you very articulately put together the mechanics of how China benefits economically from this, and I hope that your surmise of President Obama's role in this turns out to be accurate.
9/23/2013 08:40:32 pm
Wow Dave36 perfectly said and I am glad too that they posted the whole comment :)
9/24/2013 02:59:56 am
Being a daily reader of 4 dinar blogs, as I read this, I didn't find anything that I didn't already know, but I was impressed with the presentation of the information to the point that I can now have ONE article to send to someone to see if they have ANY interest in 'becoming a millionaire' before spending time and emotional energy selling them on the concept. I learned decades ago in the Amway business that when you want success for them more than they want it for themselves, the effort is like pushing a rope. Or like trying to teach a pig how to sing. (It is wasted effort and it annoys the pig.)
9/23/2013 04:30:46 pm
Wow! Awesome post thanks for the clear and concise information, finally it all makes sense. Will be soooo much easier talking to naysayers now!!!!!! Gotta love it!!!
9/23/2013 04:59:18 pm
the best yet... Wow!
9/23/2013 05:06:18 pm
Excellent information!
9/23/2013 05:08:33 pm
Well done!
9/23/2013 05:10:50 pm
Thank you for the helpful explanations and extensive research you put into this!
9/23/2013 05:13:51 pm
Down to earth, and understandable. Someone has been paying attention.
Widow Woman
9/23/2013 05:55:13 pm
Your words are wonderful. I'll be in Arizona in Oct.
9/23/2013 06:31:50 pm
So would all the encouragement from a channeled angel be true and sincere if, say, the angel was a bad one? How are you discerning between a good angel and a bad angel? How do you know this entity is lying?
9/23/2013 06:47:12 pm
tom dubose
9/23/2013 07:05:48 pm
Got to say Dave explained it better then anyone that I have been exposed too in the last 7 years. Which State was David a State Senator?. That State lost, we may have won!!
9/23/2013 07:52:06 pm
Dear Dave!!! Blessings!! An amazing , concise and clear info page packed with all the info I could not understand before...So many thanks.. Sending gratitude and warm hugs to Sedona..one of my favorites energy vortexes. You will never know how much I appreciate this message! Carmel Maguire AKA, Mammacarm
9/23/2013 07:53:53 pm
Hi David,
Diane Mattix
9/24/2013 12:10:05 am
Dave, thank you so much for the post. it explanes alot. God bless you.
9/24/2013 12:50:44 am
I would like to know who to contact to get on the Wells Fargo list. Can you please provide a name and number or email address? Thank you!
9/24/2013 02:35:09 am
Why would the banks care about taxing you if you went to another bank, this makes no sense to me. My understanding is to but your dinar in a totally separate account until they determine what the tax rate will be, the banks are not going to take on this responsibility. there are four banks participating, not just WF
9/24/2013 02:51:06 am
Dave. Loved the article. I have a friend that has 2million Dinar she got from Iraq directly when her son returned from war. They look just like mine and are not the ones with Sadams face on it. She does not want to join an email list due to her husbands job. If I give her the 800# once revealed can she get the higher rate? Pls respond to me on this
Robert Hollmann
9/24/2013 09:52:15 am
Dave, Just thought of a potentially important question---You say the (group) exchange will not be at the bank but at a separate location for security reasons, What about security there and in what form will we receive our exchange. I had been led to believe that we would have a deposit in a new account at that bank (WF) considering that we had been advised to request a non-interest-bearing account (NIB). Thank you, Bob
9/24/2013 11:55:37 am
very nice i can finally se a light at the end of a long tunnel.!!!!!thnx for the in fo awsome love az my home state thank you very much it would be nice to pay off the bills plus do lots of things for my townspeople . mesa could use some help even if it was fixing potholes in the roads!!!! thank you again.
9/26/2013 11:35:36 pm
I have subscribed to the newsletter. Does that mean I'm on the wells fargo email list. Can someone please tell me. I'm in Australia.
9/27/2013 12:11:02 am
I went to read transcript from the radio show Dave was o wed nite, it says that we are considered a group once we subscribe to this website and that this site will supply the 800#. Goggle money exchange.
Comments are closed.


text:
This trade is 8.3 months old and has likely exceeded its expiration date. It is recommended that you not consume it.
Pop Georgi | trade.tf wants to trade!
What they offer...
What they want...
Their notes...Last edited 10.1 months ago.
While you're here, you might also want to check out Pop Georgi | trade.tf's Backpack or head over to their Steam Profile. You may want to see their Recent Trades as well.
Conversation with Artu 123 (Collapse All) (Expand All)
Artu 123
[This offer has been withdrawn.]
What items are you willing to trade to Pop Georgi | trade.tf?
Steam Games


text:
Child and Adolescent Inpatient Program
This program is designed to serve youths ages 5 to 17 who are unable to be managed in an outpatient setting. The emotional, physical, and educational needs of each patient are assessed and treated. The goal of the hospitalization is stabilization. A large component to the treatment involves family therapy and involvement.
Childrens Residential Treatment Program
Our Childrens Residential Program provides 22 beds for residential treatment for children ages 6 to 12 years. During the length of stay, care is coordinated and delivered by a dedicated team of professionals including a psychiatrist, nurses, behavioral therapists, residence counselors, teachers and therapists aides.
This program has a school located onsite and provides education in a therapeutic setting. Our program also offers a strong family treatment component in order to coordinate care with the transition home. The average length of stay is 9 to 12 months.


text:
Community Development
City Hall
258 Main St
Oneonta, NY 13820
Telephone: (607) 432-0114
Fax: (607) 432-3055
Judy Pangman - Director of Community Development
Mispa Haque - Community Development Assistant
Current Initiatives
Downtown Revitalization Initiative
In 2016, the City of Oneonta was one of 10 communities in New York State to be awarded a $10 Million Downtown Revitalization Initiative (DRI) award by Governor Cuomo. The City plans to reclaim the Market Street area as a Food and Craft Beverage Innovation District, strengthen existing downtown businesses and buildings, and provide the financial resources to bring the community's transformational strategies to fruition, elevating Downtown Oneonta from good to great.
The first step in the planning process has been accomplished with submittal of the Strategic Investment Plan to NYS which identifies the City's priority projects. The State has selected projects for DRI funding (see the link to Governor Cuomo's press release, below) and program requirements will be developed soon. The City will update the public and post to this site as information becomes available.
See links below for more information:
- City of Oneonta - Downtown Revitalization Initiative
- NYS Downtown Revitalization Initiative in the Mohawk Valley
- Otsego Now – Authentic Oneonta – Downtown Revitalization Initiative
- Strategic Investment Plan
- Governor Cuomo Announces Winning Projects for Oneonta's $10M DRI
- "For Oneonta's Aging Downtown, a $10 Million Face-Lift" - New York Times, 7/24/2017
Empire State Poverty Reduction Initiative
In 2016, the City of Oneonta was one of 16 communities in New York State awarded an Empire State Poverty Reduction Initiative (ESPRI) grant by Governor Cuomo to combat poverty. The City has a very high poverty rate (29.5%), with more than 250 children under 18 years old living in poverty. The City has partnered with Opportunities for Otsego who will lead a newly created Poverty Reduction Task Force to implement Dr. Donna Beegle's Opportunity Community Model. As an Opportunity Community, the City will use the $500,000 ESPRI grant to help children and their families living in poverty break through barriers and access resources and support to move out and stay out of poverty.
Community Survey
Opportunities for Otsego has collected community input on the needs of families and individuals living in Otsego County, NY. The information will help with planning and implementation of programs to address poverty and gaps in community services.
For more information about the ESPRI program, visit Opportunity of Otsego's ESPRI page.
Brief History of Community Development Activities
The City of Oneonta has identified significant community development, housing, and economic development needs in recent years, developed improvement strategies, and successfully implemented Community Development Block Grant housing, public facilities, and economic development programs, HOME program assistance, Affordable Housing Corporation funds for First Time Home Buyer Programs, Urban Development Action Grants, and other programs to address identified needs. The programs have helped improve neighborhood target areas in the City. Programs have helped to rehabilitate almost 500 deteriorated housing units, construct over 180 low-income housing units for families, the elderly and the homeless, eliminate major public improvement problems, including water, street, and stormwater issues, and stimulate economic development, among others.
Although these actions have helped to address serious housing and economic challenges in Oneonta, the City still needs assistance, economically and physically. There clearly is a need to initiate additional economic development, downtown housing, and other improvement efforts. To help the City determine which funding programs to apply for and to help develop future Community Development initiatives, tell us about your funding needs and community development-related ideas or issues by clicking above and completing the Funding Needs Form.


text:
Hardcore interracial doggyfuck and facial of curvy whore Kleopatra Cazso
Description:Kleopatra's thick booty is made for black cocks only. That black dude with gigantic cock gets access to her great ass and pounds her like no other. When he can't hold it anymore dude covers Kleopatra's beautiful face with his black jizz.
Category:+18 only (Adult)
Added:2 years ago
18 likes, 1 dislikes
Embed / Iframe code:
Make your selection, copy and paste the embed code above.
Standart sizes: Custom size:
What is the problem?
Please do not abuse this section. The videos ,which are on investigate list, are manually checked by editor.
Security code:(is not case-sensitive) can't read
Write a comment
at least 10 characters, up to 400 characters
400 characters remaining
Security code:
(is not case-sensitive) can't read


text:
New Yorker Jacob Hadjigeorgis was practically predestined for the world of food. The son of a restaurateur, he's a guy from Queens, in his words, the "melting pot" of great cuisines from around the globe. Jacob has been passionate about food and design for as long as he can remember. Early on he spent a semester abroad in the Czech Republic, where he fell in love with art, architecture, and artisanal beer. As a student and fencing competitor he traveled widely throughout the United States, and became fascinated with regional specialties and local spices and ingredients.
In 2008, Jacob opened Mmmac & Cheese, which soon became a go-to destination for comfort food in Boston's Quincy Market. Building on his success, he set his sights back on the big apple and in December 2011 realized his dream of bringing food, drink and design to New York City by opening Jacob's Pickles on the upper west side.
Click here to see
Jacob's Pickles video,
feature on Zagat


text:
Steve Chiotakis: European stock markets are under a whole lot of pressure again today, amid fears the Greek debt crisis will spread -- and spread fast. Next door in Italy, that country's been working to raise revenues to avoid having to be bailed out by the European Union or IMF. And Italy is now looking to China for help.
From our European desk now, here's Marketplace's Stephen Beard.
Stephen Beard: The head of China's sovereign wealth fund was reportedly in Rome last week. He was there to discuss the possibility of buying Italian government bonds. That gave financial markets quite a boost. A Chinese wall of money might be just the thing to stop the downward spiral in the eurozone. But doubts are creeping in.
Steve Barrow is a currency strategist with Standard Bank.
Steve Barrow: There's a lot of speculation in the market that China has actually not committed to this. And that's putting more pressure on the Italian bond market and, as a consequence of that, on stock markets and on the euro.
He points out that there's also been talk of the Chinese buying Greek government bonds -- but that's hardly helped the Greeks. Markets indicate there's now a 98 percent chance of the government in Athens defaulting.
In London, I'm Stephen Beard for Marketplace.


text:
I've been tagged by a blogger friend and a vlogger friend--that'd be a person who makes videos as a blog, rather than a written blog like this; such a blog is usually on YouTube--to do an entry based on the following 4 scenarios:
1) An Over-Hyped book: Let's start this off with a Zombie Apocalypse! Let's say you're in a book store, just browsing, when BAM! ZOMBIE ATTACK. An announcement comes over the PA System saying that the military has discovered that the zombies' only weakness is over-hyped books. What book that everyone else says is amazing but you really hated do you start chucking at the zombies knowing that it will count as an over-hyped book and successfully wipe them out?!
2) A Sequel: Let's say you've just left the salon with a SMASHING new haircut and BOOM: Torrential downpour. What sequel are you willing to use as an umbrella to protect yourself?
3) A Classic: Let's say you're in a lecture and your English teacher is going on and on about how this classic changed the world, how it revolutionized literature and you get so sick of it that you chuck the classic right at his face because you know what? This classic is stupid and it's worth detention just to show everyone how you feel! What Classic did you chuck?
4) Your least favourite book of life!: Let's say that you're hanging out at the library when BAM global warming explodes and the world outside becomes a frozen wasteland. You're trapped and your only chance for survival is to burn a book. What is the book you first run to, your least favourite book of all life, what book do you not fully regret lighting?
These four scenarios originated on YouTube by Ariel Bissette, and she explains it way better than I could. Watch that video here: http://youtu.be/Z_2UxYi8fOA.
So, the disclaimer: These are just my opinions. Can I say that again? These are just my opinions! (I was gonna put that all in caps, but that's rude.) One of the coolest things about books is that people get very, very, very serious about them. They will get offended by the opinions of others. Books can be so personal! So I get that. And I dig that. But that's why my opinions are strongly felt, too. You don't have to agree with them! That's the point!
If you disagree or if you agree, let me know. Feel free to answer these in a comment, or in your own blog.
And I gotta add: I was so PISSED at the following vlog that I almost left a comment! The vlog is from a usually-amusing and creative and smart, and always energetic vlogger named Christine Riccio. She has a vlog about books, where she talks a lot about a book, and reviews it and rates it, and she really gets into what she's read. Anyway, in her Book Sacrifice, she said that the classic she thought was terrible was The Catcher in the Rye, and she slams it. This book was Mark David Chapman's favorite (he shot John Lennon, if you're too young to know), but so what? Lots of religious books are the faves of killers past and present, so don't make me go there. Anyway, the specific vlog of hers referenced here is at this site: https://www.youtube.com/watch?v=0pEK25Z7PPs so you should see it. And I didn't leave a comment because, well, have you read the negative comments that losers leave on internet articles and YouTube videos? I mean, are you kidding me?!? Why do these people not have anything else better to do? Anger and bitterness are nasty, nasty things!
My answers:
photo: from the book's Wikipedia page
1. An over-hyped book I'd clobber a zombie with? (Does that mean it has to be big enough to be used as a weapon?) Well, where do I start? I have to say...Just about any John Green book. Great philosophical ideas and themes, so-so writing. And often books based on philosophical concepts (which most of his are) do not translate well into print, because you have to create a plot for them. Doing that for philosophical concepts can be slippery and metaphysical. Like, you can't touch it. Example: The Fault in our Stars. Two teens with life-threatening diseases are trying to keep it real, and are looking for the meaning of life, or just plain Meaning in general. They find it in the seemingly-real work of an author who turns out to be a boozing butthole, who is not his persona, who does not keep it real, who is in fact just a real jerk. Okay, except...can two teens with these diseases and cancer really travel that far? And don't get me started on Looking for Alaska. I know John Green is huge in the YA and teen world, and that's very cool. Keep reading him! (Just don't ask me to.) I'd throw other YA titles here, like any of the Twilight (You don't fall in love with vampires! You kill them! They're evil! They're not good for dates, or to introduce to your parents, or to take to Sunday dinner!) or Divergent series. And any Nick Sparks book.
photo: from the book's Wikipedia page
2. The worst sequel of all time is Doctor Sleep, the awful, shitty, boring, badly-written travesty of a sequel to the pitch-perfect classic The Shining. I can't tell you how angry this book made me. It sucked! Danny of The Shining turned out to be this?!? Are you shitting me? And Jack Torrance turning up at the end to push her off the cliff? And she screams "F--- you" as she falls? How...base! ARGH! I normally love Stephen King books. I've read them all and I still have them all. But when he's bad, Oh My Lord...
A close runner-up here would be the sequel to To Kill A Mockingbird. This manuscript was sent to the publisher by Harper Lee's money-grubbing agent, and she found it in Harper Lee's sister's safety deposit box. Harper Lee had had a stroke and late-onset dementia when she signed the papers to publish this. I'm thinking she had no idea of what she was signing. She infamously published that one book, despite offers of millions of dollars to publish others. Would she not publish for over 50 years and then do so on her deathbed? And the iconic, peace-making Atticus Finch as an old, angry racist?!? Are you shittin' me?!? And why was this found in Harper Lee's sister's safety deposit box? The murder / mystery fan in me thinks it was because her sister thought she'd publish it and make millions if Harper Lee died first...but she didn't! I'll bet Harper Lee had no idea where this manuscript was, that it was long gone and long lost. It's actually the book that was going to be Mockingbird, but the publisher thought it was too negative and suggested she write something else, so she wrote what became Mockingbird. So it's actually just an early draft! That a publisher allowed this to be made and tarnish the genius of her actual, only published book. A TRAVESTY!!! I haven't read it, and never will. I know someone who's an English teacher, and she's married to a lawyer, and they named their son Atticus (yes), and even she refuses to read this. Luckily for her son, most people will never associate his name with the guy from this book!!!
photo: Charles Dickens, from his Wikipedia page
3. The worst classic? I couldn't finish The Lord of the Rings until I saw the movies first. Tried a great many times. But a lot of it was good. I stalled at the Tom O'Bedlam part, or whatever he was called. Never even appeared in the movies. Anything by Charles Dickens. I've tried to get through A Christmas Carol. Still can't do it. I tried reading all of A Tale of Two Cities. Still can't do it. The sentences are just too damn long. Great individual paragraphs--notably the first and last, a classic example of bookending--and the last scenes are classics. That's how we should read Dickens today--just the classic scenes.
Why so many words?
Because he originally published his novels as serials in magazines.
And he owned the magazines.
And he paid by the word.
photo: from the book's Wikipedia page
4. My least favorite book of all time? See #2. Throw Rose Madder there, too. I stopped reading that one when this woman sat on the bad guy and peed on him. Yes. Books that were so bad they made me actually angry. Like, strike someone across the face angry. I'm an angry bitter little man and I don't care. I once read a mystery / cop novel, when I first started the 20th draft of Cursing the Darkness, I forget the title now--::tries remembering title, even keywords to Google it, but can't--and it was sooooooooo bad. Sentences like: "I got the call to go to the murder site. But I first finished my dinner. Funny how these always happen during dinner. And the dead aren't going anywhere." Are you f---in' sh---in' me?!? I mean, how bad does writing have to be to be published, anyway?!? So laughable I couldn't get angry because it was just sooooooooo bad!!!
So, those are my answers. What say you? Comment, or email, or write your own blog--whatever!
No matter what, keep reading!
Thanks for reading my blog! Bye!


text:
Thank you to everyone who has expressed their good wishes over the past few weeks.
We want to let everyone know that we will be holding an informal memorial celebration in honor of the life of José Joni Argueta Hernandez. It will be held on Monday, May14th, beginning at 8:30pm, here at Adega. All who wish to remember Joni are welcome to attend.
With our best,


text:
De Merode, head of Congo's Virunga National Park, recovering from attack
Unidentified armed men have critically wounded the Belgian head of Africa's oldest wildlife reserve, the Virunga National Park in Democratic Republic of Congo, officials said.
The victim, Emmanuel de Merode, "was shot in the chest", North Kivu provincial governor Julien Paluku said on Tuesday, following the attack, which took place about 30 kilometres north of the capital, Goma.
Belgian Foreign Minister Didier Reynders tweeted his best wishes for De Merode's swift recovery, adding that "we are opening an enquiry", into the apparent ambush.
A Congolese army official also said that an investigation was under way.
Paluku said the attack happened as De Merode was driving himself, unescorted, from Goma towards the Congolese Institute for Conservation and Nature centre in Rumangabo.
De Merode was in hospital in Goma following an operation to remove bullets from his body.
The Virunga reserve, on the border with Uganda and Rwanda, covers 800,000 hectares and has attained worldwide renown, notably for its rare and endangered mountain gorillas. The area is exceptionally rich in biodiversity, but is located in the scarred North Kivu province, tracts of which have been ravaged by successive conflicts for more than 20 years.
Poachers and logging teams have damaged the reserve, but the park is also criss-crossed by rival armed groups and soldiers, while local people have taken up illegal residence.
Most Popular
- 1
- 2
- 3
- 4
- 5
- 1
- 2
- 3
- 4
- 5


text:
Limp Bizkit, Creed and The Strokes are the unlikely acts at the top of music magazine GUITAR WORLD's Worst Bands of 2003 poll.
The groups were one, two and three on the list, with "all pop punk bands" coming in at number four and Good Charlotte at number five.
Metallica's ST ANGER album was named the Disappointment of The Year in the poll, but the project was also named the second best album - behind THE BLESSED HELLRIDE by Black Label Society.
Metallica's Kirk Hammett was named Best Metal Guitarist and Foo Fighters star DAVE GROHL Best Rock Guitarist.
Led Zeppelin's HOW THE WEST WAS WON package was picked as the Rock Album of 2003, beating out THE WHITE STRIPES' ELEPHANT, which topped many December (03) album polls.05/01/2004 18:10


text:
We help children stay safe online. Has someone acted inappropriately towards you online, or to a child or young person you know? It may be sexual chat, being asked to do something that makes you feel uncomfortable or someone being insistent on meeting up. You can report it to us below. https://www.ceop.police.uk/Ceop-Report/
Need immediate help?
Do you need immediate help or have a real emergency? If so call 999 or contact your local police here: https://www.police.uk/hertfordshire/D01/
For more information please visit the CEOP website http://www.ceop.police.uk/
This is an assembly from CEOPs Thinkuknow education programme that enables young people to recognise what constitutes personal information. The assembly facilitates young peoples understanding that they need to be just as protective of their personal information online, as they are in the real world. It also directs where to go and what to do if young people are worried about any of the issues covered.


text:
Home > Arts & Events >
Steinway Piano Factory
1 Steinway Pl.,
Queens, NY 11105
In 1853, Henry Engelhardt Steinweg and his five sons introducedand eventually patentedacoustic and mechanical improvements that made their grand and upright pianos exemplars of craftsmanship. Maintaining that reputation, sometimes at the expense of market share and profits, has been the company's singular obsession ever since. It still takes a year to make a Steinway, which is made the same way, and in the same factory, as it has been for more than a century. Steinway is the sole American piano maker left (and one of the last major manufacturers in New York City). Since its 1872 opening, what once fostered a 400-acre company town has been whittled down to one four-floor factory complex. Here, the 2,000 pianos turned out yearly are almost entirely hand-made by Steinway's 300 craftspeople, some of whom learned the trade alongside their parents. They saw, sand, bend, carve, and regulate the 12,000 parts of each instrument with tools and machines that were used by 19th century workers. Inventory is still kept with paper and pencil; new processes like the "Pounding Room," where a machine bangs on the keys thousands of times to reveal any flaws, have been introduced to further guarantee time-honored quality.Steinway Village
The old Steinway Village surrounding the factory once featured schools, post offices, and shops. Many of these buildings are still standing; the original workers' rowhouses can be seen on 20th Ave., between 41st and 42nd Streets. The Steinway Mansion is on the corner of 42nd Street and 19th Avenue.
Offered in the fall, winter and spring, the free 2.5-hour tour begins at 9:30 a.m. in the lumber yard and follows the path each piano takes to completion. Highlights include the sauna-like curing room, a vault stacked with precious veneers, and the famous rim-bending room where burly workers force lengths of wood into piano-shaped moulds. Advance reservations are required; email firstname.lastname@example.com or call 718-721-2600 x3169.