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The time course of the autoregulatory response of renal blood flow (RBF) to a step increase in renal arterial pressure (RAP) was studied in conscious dogs. After RAP was reduced to 50 mmHg for 60 s, renal vascular resistance (RVR) decreased by 50%. When RAP was suddenly increased again, RVR returned to baseline with a characteristic time course (control;n = 15): within the first 10 s, it rose rapidly to 70% of baseline (response 1), thus already comprising 40% of the total RVR response. Thereafter, it increased at a much slower rate until it started to rise rapidly again at 20–30 s after the pressure step (response 2). After passing an overshoot of 117% at 43 s, RVR returned to baseline values. Similar responses were observed after RAP reduction for 5 min or after complete occlusions for 60 s. When tubuloglomerular feedback (TGF) was inhibited by furosemide (40 mg iv, n = 12),response 1 was enhanced, providing 60% of the total response, whereas response 2 was completely abolished. Instead, RVR slowly rose to reach the baseline at 60 s (response 3). The same pattern was observed when furosemide was given at a much higher dose (>600 mg iv; n = 6) or in combination with clamping of the plasma levels of nitric oxide (n = 6). In contrast to RVR, vascular resistance in the external iliac artery after a 60-s complete occlusion started to rise with a delay of 4 s and returned to baseline within 30 s. It is concluded that, in addition to the myogenic response and the TGF, a third regulatory mechanism significantly contributes to RBF autoregulation, independently of nitric oxide. The three mechanisms contribute about equally to resting RVR. The myogenic response is faster in the kidney than in the hindlimb.
- renal hemodynamics
- tubuloglomerular feedback
- myogenic response
although many factors may modulate autoregulation of renal blood flow (RBF) (38), the basic function is presently believed to derive from only two underlying mechanisms: the myogenic response and tubuloglomerular feedback (TGF) (3, 23, 38, 48). However, there is no simple way of eliminating the myogenic response without affecting the TGF at the same time. Therefore, the contribution of the myogenic response has so far been deduced only by means of exclusion from the degree of autoregulation, which is left after blockade of the TGF by direct interruption (32, 44), clamping (42) of tubular flow, ureter occlusion (14,41), or furosemide (2, 30, 37). Due to these experimental constraints, it cannot be excluded that the remnant autoregulation after blockade of the TGF comprises further regulatory mechanisms in addition to the myogenic response. Accordingly, it is not clear today whether mechanisms in addition to the myogenic response and the TGF contribute to the autoregulatory process.
The response times of the myogenic response and the TGF differ considerably from each other. Although in the kidney the myogenic response seems to reach its maximum effect within a few seconds after activation (10, 12, 21, 30, 53), TGF comprises a delay of 10–20 s (7, 13) and requires 1–2 min to achieve its full response (6, 7, 13). Therefore, it is possible to dissociate both mechanisms by their distinct temporal characteristics. This has been done successfully already by studying the transfer function (2, 12, 14, 21, 30) and by analyzing the autoregulatory response to a step increase in perfusion pressure (24, 40, 43, 45, 51, 53). Transfer function studies have shown that although active under physiological conditions (2, 12,14, 21, 30), the TGF is not required to explain the limited autoregulatory strength, which is observed under these conditions (2, 14, 30). However, the transfer function does not allow for assessment of the actual contribution of the TGF under resting conditions. Although to some extent this would be possible by a step function analysis, the available studies have not directly made use of this feature and were limited to anesthetized animals (24, 43,45, 49, 53) and the artificially perfused kidney (40,51).
The response time of the myogenic response in renal vessels (3–10 s) is considerably faster than that in other vascular beds (30–120 s), such as those in skeletal muscle (16, 18,25), brain (35, 39), and skin (15,34). Although these temporal differences have been experimentally investigated by studying the renal and the mesenteric circulation (1) and discussed in a recent review (20), a direct comparison with other vascular beds to our knowledge has never been done, except for a cursory notion in the original work of Bayliss (5) and a step function analysis in artificially perfused organs (31).
Therefore, the purpose of the present study was threefold:1) to investigate the step response of RBF autoregulation in the conscious dog to dissociate the myogenic response from the TGF and to test whether further mechanisms with still other response times may be involved; 2) to estimate the relative contribution of each mechanism to the autoregulatory adaptation of vascular tone under resting conditions; and 3) to compare the temporal pattern of the responses in the renal vessels to those in the hindlimb vasculature.
In accordance with the national guidelines for the care and use of research animals (Reg.Präs. Karlsruhe license 37–9185.81/156/96), 66 experiments were made in 18 conscious foxhounds (27–37 kg). The dogs were held under an artificial 12:12-h light-dark-cycle and were fed a standard dog diet (SSNIFF Spezialdiäten, Soest, Germany) with free access to tap water.
Chronic Instrumentation
The dogs were surgically prepared under sterile conditions. After premedication with atropine (0.5 mg sc; Braun, Melsungen, Germany) and propionylpromazine (Combelen, 0.5 mg/kg sc; Bayer, Leverkusen, Germany), anesthesia was induced by pentobarbital sodium (Nembutal, 20 mg/kg; Sanofi, Libourne Cedex, France) and maintained by halothane (Fluothane, 0.8–1.0%; Zeneca, Planckstadt, Germany) and N2O (0.5 l/min). The depth of anesthesia was checked by repeated testing of the eyelid reflex. At induction, masseter relaxation was also assessed. Via a left-flank incision, a polyurethane catheter was implanted into both the abdominal aorta and the left renal artery. An ultrasonic transit-time flow probe (type 6SS, Transonic, Ithaca, NY) was also mounted on the left renal artery. To allow a controlled reduction of renal arterial pressure, an inflatable vascular occluder was placed on the same artery distal to the flow probe. A Silastic catheter was implanted into the left renal vein for the infusion of drugs. Three dogs received no venous catheter. In these animals, the infusions were made through a cannula inserted into a limb vein at least 10 min before the experiment was started and removed afterward. To also assess the adaptive responses in the hindlimb circulation, in five dogs a flow probe (type 8RS, Transonic) and a vascular occluder were implanted on the left external iliac artery in a separate procedure through a transperitoneal approach after a midline abdominal incision under the same type of anesthesia. In three dogs, this was done after all experiments on the renal artery had been completed; the other two dogs were only subjected to the iliac implantation procedure without prior perirenal surgery. In these animals, the aortic catheter was implanted during the same iliac surgery. Catheters and cables were subcutaneously led to each animal's neck, where they were exteriorized. At least 10 days were allowed for recovery before experiments were started. On the day of surgery and ondays 3 and 6 thereafter, the dogs received a combination of benzylpenicillin and sulfatolamide (Tardomycel, 3 ml sc; Bayer). The catheter was flushed every second or third day and filled with a solution of heparin (1,700 IU/ml) in 0.9% saline. In some of the dogs this solution also contained cephtazidim (Fortum, 16 mg/ml; Glaxo, Bad Oldesloh, Germany) as described in more detail previously (4).
All experiments were made between 7:30 and 11:30 AM while the dogs were resting on their right side as trained before. Arterial pressure in the aorta (AP) and in the renal artery (RAP) were measured from the two catheters by pressure transducers connected to amplifiers (Statham P23XL with Gould Pressure Processor, Gould, Valley View, OH). RBF was obtained by an external flowmeter (Transonic T106 or T108) connected to the implanted flow probe. The output of the flowmeter was low-pass filtered below 10 Hz by the built-in analog filter. In most of the experiments the air pressure used to control the vascular occluder was measured by a pressure transducer (BTE 4005G0, Sensor-Technics). All data were recorded continuously on a computer at 20 Hz (for more detail, see Refs. 28 and 30). This measurement equipment provided adequate dynamic characteristics for the purpose of the present study. The frequency response of the catheter-transducer system provides accurate transduction up to 1 Hz, and −3-dB attenuation above 3 Hz (30), corresponding to a time constant of 53–159 ms. The frequency response of the RBF signal was limited only by the low-pass filter and the sampling frequency.
Pressure reduction.
To investigate the adaptive changes in renal vascular resistance (RVR) in response to a sudden increase in perfusion pressure, RAP was reduced to 50 mmHg for a duration of 60 s and was then suddenly restored to aortic AP. The reduction of RAP was achieved by inflation of the implanted occluder with room air controlled by hand with a 50-ml syringe while RAP was observed on a paper recorder (Gould 2600). This procedure is herein referred to as pressure reduction. Usually, RAP was restored almost immediately after reopening of the artery, at the latest with the next systole (see also Fig.1 A). If this was not the case, the response data were discarded. Under each experimental condition, at least three such pressure reductions were made, succeeding each other in intervals of 10 min, thus allowing intercalated recovery periods of 9 min. Periods of 4 min were also used in the case of high-dose furosemide to allow measurements at an early time point after the drug, and periods of 14 min were used after prolonged pressure reductions to allow longer recovery (see below). In eight dogs under control conditions, additional pressure reductions were conducted, during which the renal artery was completely occluded. In the case of technical insufficiencies of a pressure reduction or complete occlusion (e.g., failure to keep RAP constant, slow rise in RAP after reopening, movement or deep breath by the dog during the response), an additional reduction was made after the respective recovery time. At the end of each experiment, the renal artery was completely occluded for 30 s to obtain the zero-flow offset. In the case of iliac blood flow (IBF), the same protocol was followed, but because no catheter was available distal to the occluder, the artery was completely occluded for 60 s.
Experimental conditions.
Each experiment, except for the complete occlusion and high-dose furosemide, was conducted on a separate day. The order of the experiments made in an individual dog was randomly assigned. After furosemide or N G-nitro-l-arginine methyl ester hydrochloride (l-NAME), 1 wk was allowed for recovery. Not all experiments were done in each individual, but a control experiment was done in every dog.
After a resting period of 10 min, three pressure reductions (n = 15) were made in intervals of 10 min, i.e., 10, 20, and 30 min after the start of the recording (see also Fig. 2, Table 1).
In eight of the control experiments, after a recovery period of 19 min after the last pressure reduction, three additional reductions were performed (n = 8), during which the artery was completely occluded for 60 s, with intercalated recovery periods of 9 min (see Table 1).
After a resting period of 10 min, two to three pressure reductions were made (n = 7), during which RAP was reduced to 50 mmHg for a period of 5 min instead of 60 s. Fifteen minutes were allowed for recovery after each pressure reduction (see Table 1).
After a resting period of 10 min, furosemide (n = 12) was injected (Lasix, 40 mg iv; Hoechst Marion Roussel, Frankfurt, Germany). Pressure reductions were made at 15, 25, and 35 min after furosemide (see Table 1).
After a resting period of 10 min, five pressure reductions were conducted (n = 6) under control conditions at 10, 20, 30, 35, and 40 min after the start of the experiment, i.e., with intercalated recovery periods of 9 min between the first three and 4 min between the last three pressure reductions. Nine minutes after the last pressure reduction, furosemide was injected (20 mg/kg iv; i.e., >600 mg). Pressure reductions were made at 5, 10, 15, 25, and 35 min after furosemide (see Table 1).
After a resting period of 10 min, the nitric oxide (NO) synthase inhibitor l-NAME (50 mg/kg iv; Sigma, Deisenhofen, Germany) was slowly injected (n = 6). Then, 45 min later, the NO donorS-nitroso-N-acetyl-dl-penicillamine (SNAP; Alexis, Grünberg, Germany) was infused (4 μg · kg−1 · min−1 iv) in 12 ml/h of vehicle (11.06 ml/h saline+40 μl/h of DMSO). Forty-five minutes after the start of SNAP, furosemide was given (40 mg iv). Pressure reductions were made at 15, 25, and 35 min after furosemide (see Table 1).
To obtain preliminary information about a possible involvement of the renin-angiotensin system, further experiments were made in three dogs, in which the responses after furosemide were tested in the additional presence of clamping of ANG II plasma levels. Thirty minutes before the start of the recording, an oral dose of the angiotensin-converting enzyme inhibitor ramipril (2 mg/kg, donated by Hoechst Marion Roussel) was given. Ten minutes after the start of the recording, an infusion of ANG II was begun at a constant rate (5 ng · kg−1 · min−1 iv in 10 ml/h saline). After an additional 10 min, furosemide was given (40 mg/kg iv). Pressure reductions were induced at 35, 45, and 55 min after the start of the recording, i.e., at 15, 25, and 35 min after furosemide.
After a resting period of at least 10 min, the external iliac artery was occluded for 60 s (n = 5). This was repeated two to four times with recovery periods of 5–15 min. To test for possible metabolic effects, in two dogs additional occlusions were made in the same experiment, during which the artery was either completely occluded for 30 s or only partially occluded (IBF reduced but not stopped) for 25 s and then completely occluded for the final 5 s before being reopened. The order of the different types of pressure reduction was randomly assigned.
Data Analysis
The original 20-Hz data of RBF and RAP were smoothed by a sliding average over 40 values (2 s). RVR was calculated from the smoothed data of RBF and RAP by dividing (RAP − RAP0) through (RBF − RBF0), where RAP0 is the pressure at which RBF ceases, and RBF0 is the zero-flow offset. A value of 16 mmHg was assumed in all cases for RAP0, which is the average value found in the experiments in the present study with complete occlusion. In the first 27 experiments, in which the air pressure was not recorded, the exact time points of the beginning and end of the periods of reduced RAP were determined by visual inspection of the original 20-Hz RBF and RAP data. After an appropriate pressure transducer was made available in the following experiments, the 20-Hz signal of the air pressure in the occluder was used for automatic detection of the time points. On the basis of these time points, the time courses of the responses to all pressure reductions of an experiment were averaged. Trials with technical insufficiencies (see above) were discarded. For each experimental group a mean curve was calculated from the averaged time courses of all dogs. In addition, for each pressure reduction the following features of the time course of RVR were determined automatically (see Fig. 1 A, thick horizontal bars) as follows: baseline (BASE in Fig.1 A) is the mean from the last 60 s before the pressure reduction; minimum resistance (MIN in Fig. 1 A) is the mean from the initial 2.5 s after release; maximum of response 1 is the maximum found between 2.5 and 10 s after release after further smoothing by sliding average over 40 consecutive values; plateau (PLAT in Fig. 1 A) is the mean from 10–25 s after release; and maximum of response 2 is the maximum found between 25 and 80 s after release after further smoothing by sliding average over 40 values. To estimate the relative contribution of the first and the second rise in RVR to the total autoregulatory response, the rise of RVR from MIN to PLAT was expressed as the percentage of the total response between MIN and BASE [PLAT%= (PLAT − MIN)/(BASE − MIN) ∗ 100]. The same normalization to the total response was made for all RVR values of the time courses of each individual pressure reduction (Fig. 3). Vascular resistance in the external iliac artery (IVR) was calculated from the smoothed data of aortic AP and IBF similar to the calculation of RVR, except that 0 mmHg was assumed for venous pressure [AP/(IBF − IBF0)]. Heart rate was determined off line, beat by beat from the 20-Hz AP signal.
The effects of the experimental interventions were determined by comparison with the respective values from the paired control experiments on the same individual. Statistical significance of these differences was tested by one-way ANOVA for repeated measures including all groups followed by a Student-Newman-Keuls test using Sigmastat 2.03 (SPSS, Chicago, IL). Normality was tested by a Kolmogorov-Smirnov test, equality of variances by a Levene median test. If one of the latter tests failed, Kruskal-Wallis one-way ANOVA on ranks was used followed by Dunn's method of comparison. In all cases, a P value of 0.05 was considered significant. All values are expressed as means ± SE.
The typical time course of RAP, RBF, and calculated RVR during one of the pressure reductions is depicted in Fig. 1. During the reduction in RAP (Fig. 1 A), RBF (Fig. 1 B) initially dropped considerably, but in the following time period it partially recovered. This autoregulatory behavior is reflected by an almost exponential decrease in RVR (Fig. 1 C) during this period. With the subsequent step increase of RAP back to the systemic AP, RBF initially rose above the preocclusive level and then recovered from this reactive hyperemia in a characteristic manner.
Figure 2 A shows the averaged time course of RVR of the control experiments from all 15 dogs. For the sake of simplicity, the data segment containing the RAP reduction has been eliminated in this and Figs. 3 and 4. Thus time 0in these figures corresponds to the time of the release of the pressure reduction. Positive numbers on the time scale refer to the time after release, whereas negative numbers denote the time before the beginning of the pressure reduction. The relatively large variation in RVR among the dogs mainly derived from differences in the resting level of RBF (Table 2). Accordingly, the error range of the mean curve was much smaller when the single curves were expressed as the percentage of the individual preocclusive level (Fig.3).
During the 60-s period of RAP reduction, RVR decreased from 0.33 to 0.17 mmHg · ml−1 · min (see Table3). This corresponds to almost exactly one-half of the preocclusive value (51.0 ± 1.2%). From this level, RVR rose back to control in at least two successive steps: within the first 10 s it rapidly increased to 70.7 ± 1.3% of the preocclusive level (Fig. 2 A). This is referred to in the following discussion as response 1. In some cases this response showed a small overshoot, but on average it reached only 98 ± 2% of the following plateau phase of RVR. During the subsequent 10–20 s, the rise continued at a much slower rate (Fig.2 A). This is referred to as the "plateau." After a delay of 20–30 s after the pressure step (Fig. 2A), response 2 began. Because of the applied smoothing procedure, a more exact determination of the beginning of this response was not possible. Almost in every instance it displayed an overshoot, which, on average, reached 122 ± 4% of the preocclusive level and occurred at 45 ± 2 s after release of the occlusion.
To estimate a possible contribution of metabolic factors to this time course, additional experiments were conducted, during which the period of RAP reduction was either prolonged for 5 min or the renal artery was completely occluded for 60 s. After prolonged pressure reductions, the occurrence of the maximum of response 2 was significantly delayed by 20% (54 ± 4 vs. 45 ± 2 s,P < 0.01: Fig. 2B). After complete occlusion, the time course appeared similar (Fig. 2), although it took up to 5 min for RVR to completely return to the baseline level (data not shown). In addition, both the onset (∼40–50 s after reopening; Fig. 2) as well as the maximum (74 ± 2 vs. 41 ± 2 s,P < 0.001; Fig. 2) of response 2 were delayed, whereas the magnitude of its maximum was slightly attenuated (88 ± 2 vs. 119 ± 3% of baseline RVR, P < 0.05).
Neither the smallest resistance at the end of the pressure reduction or complete occlusion (Table 3) nor the level of RVR during the plateau (Table 3) displayed any appreciable difference from the values found after 60 s of RAP reduction. These characteristics of the response, therefore, seem to be robust and largely independent of time and metabolic factors. Nevertheless, to keep confounding influences small, all other experiments were conducted with a pressure reduction for 60 s.
To test the possibility that capacitative effects due to pressure-induced changes in kidney volume might produce apparent changes in RVR, step changes in RAP were induced between 30 and 50 mmHg, i.e., below the pressure range of active autoregulation (data not shown). In this experiment, changes in RVR were seen after the pressure steps, compatible with capacitative effects. However, these were smaller than response 1 of RVR (∼ 50%) and were completed after <20 s.
To investigate the contribution of the TGF to the observed response, experiments were conducted after administration of furosemide. Although mean RBF increased transiently after furosemide (data not shown), by the time of the pressure reductions (after 15 min) it had returned to its control level. Under these conditions, the minimum vascular resistance after the pressure reduction was neither in absolute values (Table 3) nor relative to the preocclusive level (56 ± 1 vs. 50 ± 1%), significantly different from the values obtained under control conditions. This indicates that the maximum capacity for pressure-dependent vasodilatation was significantly, but only slightly, attenuated. In contrast, the time course of RVR after release of the pressure reduction was significantly affected: although response 1 was enhanced so that RVR reached a higher level during the plateau (Table 3), response 2 was completely abolished (Fig.3 A).
To facilitate an estimation of the relative contribution of the different responses to the total regulatory change in RVR, it was normalized to the difference between the preocclusive baseline level and the minimum RVR after the pressure reduction (see alsomethods). This demonstrates that RVR reached 39 ± 2% of its total response during the plateau under control conditions, whereas it rose to 60 ± 3% after furosemide (Fig.3 A). This difference was highly significant (P < 0.001). Nevertheless, even after furosemide, RVR during the plateau was still clearly <100% of the total response (Fig. 3 A), demonstrating that response 1 did not reach sufficient strength to elevate the plateau of RVR all the way back to the preocclusive level (Table 3, Fig. 3 A). In contrast, after furosemide RVR further increased from the plateau in a slow rise to reach the baseline level after 68 ± 2 s, i.e., significantly later than under control conditions (45 ± 2 s,P < 0.001).
One simple explanation for these observations might be a dose of furosemide too small to completely eliminate the TGF. For this reason, experiments were made during which a much higher dose of furosemide was applied. Again, during the plateau, RVR did not reach the baseline level (Table 3) but only rose to 70 ± 5% of the total response compared with 46 ± 2% in the paired controls (P< 0.001). The same result was obtained when the pressure reductions were conducted at 5, 10, and 15 min after furosemide, when the plasma concentrations are expected to be highest (RVR during the plateau was 69 ± 6% of the total response). This was also similar to the plateau of RVR after the lower dose of furosemide in the same dogs (67 ± 4%).
These results indicated that not two but three regulatory mechanisms with different time courses contribute to RBF autoregulation. To investigate whether the slow rise in RVR after furosemide, i.e., the third mechanism, might derive from an adaptive release of endogenous NO, experiments were made during which plasma levels of NO were clamped. Under these conditions (Fig. 3 C) there was a prominent augmentation of the overshoot of response 1 (143 ± 9 vs. 89 ± 3% of RVR at the plateau, P < 0.001). Nevertheless, RVR did not reach the baseline level during the plateau (Table 3, Fig. 3 C) but rose to 61 ± 2% of the total response under furosemide compared with 67 ± 4% after furosemide alone and 46 ± 2% (P < 0.01) without administration of any drug, in the same group of dogs.
Additional experiments in three of the dogs showed that also after furosemide in combination with clamping of the plasma levels of ANG II, RVR during the plateau reached only 64 ± 6% of the total response, compared with 66 ± 7% after furosemide alone and 46 ± 4% without use of any drug in the same animals. Thus restoration of RVR during response 1 after the pressure step appears to be independent of changes in ANG II plasma levels.
The rapid time course of response 1 seemed surprising in view of the known response times in other vascular beds. Therefore, similar experiments were conducted on the external iliac artery in five dogs of the same strain. IVR was 0.58 ± 0.08 mmHg · ml−1 · min before the occlusion and fell during the occlusion to ∼30% of this baseline. From this level, it did not rise appreciably during the initial 4–6 s and then only slowly increased to reach the baseline level, but not before 20–30 s after release of the occlusion (Fig. 4, thick solid line). This time course was not substantially different if the occlusion lasted only 30 s (Fig. 4, thin solid line) and even if the artery was partially occluded for 25 s and then completely occluded for only 5 s (Fig. 4, thin dotted line). In contrast, in the response in the renal circulation after 60 s complete occlusion during furosemide, RVR fell to only 50% of the baseline value and then rapidly increased in response 1, already reaching its maximum 4–6 s after reopening of the artery.
The present study demonstrates the temporal characteristics of the myogenic response and TGF and their contribution to resting vascular tone in the kidney. In addition, the results strongly suggest the participation of a third, previously unrecognized mechanism in the autoregulation of RBF. Under resting conditions, ∼50% of the basal vascular tone is available for autoregulatory vasodilatation, to which all three mechanisms seem to contribute by approximately equal amounts. Finally, direct comparison with the autoregulatory response in the hindlimb circulation shows that the myogenic response in the kidney is substantially faster than that in skeletal muscle.
Time Course
The averaged time courses show that RVR adapts to a step increase in RAP in three steps with differing temporal patterns. At least the two faster responses are in perfect congruence with previous observations of the responses to a step rise in RAP (40, 43, 45,51, 53), although in one of these studies (24)response 1 and thus the plateau were not overtly discernible.
Response 1, which reaches its maximum within the first 10 s after the pressure step, most probably comprises the myogenic response. Although no direct proof is possible, the most compelling evidence for this view is the pronounced similarity of the time course to that observed in rats after a rapid reduction of perirenal pressure (10). The vasoconstriction observed under the latter conditions can hardly be explained by mechanisms other than a myogenic response. The scarce occurrence of an overshoot of this response in our study is also in line with the findings by Clausen and co-workers (10). Because an overshoot can only be generated in a control system higher than first order, i.e., including a rate-sensitive component, the results suggest that the latter is not prominently active under these conditions. The same conclusion was drawn from the phase relationship of the transfer function between RAP and RBF (30) and is also in line with direct observations in isolated hamster cheek pouch arterioles (15). The overshoot was enhanced under furosemide, and even more so during additional clamping of the plasma levels of NO levels. Similar enhancements of the myogenic response and its dynamics have also been observed after furosemide (10) or NO synthase inhibition (26, 50).
Response 2, which started 20–30 s after the pressure step and almost always presented an overshoot at 40–50 s, not only largely resembles the temporal characteristics of the TGF observed in micropuncture experiments (6, 7, 13) but was also abolished by furosemide, which is known to block the TGF. The observed enhancement of this response after prolonged pressure reduction might be due to activation of the renin-angiotensin system with subsequent production of ANG II, which is known to augment the gain in TGF (38). The reduction of the maximum RVR of response 2after complete occlusion might be explained by an additional depression of RVR by metabolic factors or by prolonged activation of a third response (response 3) induced by the complete occlusion. The slowing of this response might be caused by a more complete emptying of the tubuli than during the pressure reduction to 50 mmHg, leading to a further delay in the reinitiation of distal tubular flow.
After blocking of the TGF, response 3 becomes apparent, which comprises a slow rise in RVR, reaching the baseline level after 60 s. It is very unlikely that this represents a remnant function of the TGF due to an insufficient dosage of furosemide, because exactly the same changes in RVR were found after an extremely high dose of furosemide. Although the actual concentration of furosemide at the macula densa is not known, measurements of its concentration in the urine in similar experiments in a previous investigation from this laboratory (30) have suggested sufficient concentrations even after a dose of only 10 mg/kg. There was also no indication for any dose dependency with the two doses of furosemide used in the present study. The observation that under control conditions RVR slowly increased during the plateau at an almost identical rate as the slow rise after furosemide suggests that the third mechanism is active also in the absence of furosemide, i.e., when the TGF is intact. Although it cannot be entirely excluded that part of response 3 may actually arise from capacitative effects due to slow changes in kidney volume, the observed changes in RVR after pressure steps between 30 and 50 mmHg do not seem large and slow enough to fully explain its time course. However, there is no simple way to assess capacitative effects in the normal pressure range. It seems noteworthy that a corresponding slow adaptation of RBF during the plateau phase under control conditions can also be detected in the data of previous publications (45, 53), although the authors did not explicitly mention this feature. Furthermore, in the transfer function between RAP and RBF, a small peak in the gain spectrum was observed, ∼0.016 Hz (i.e., with a cycle length of 60 s) in the presence of furosemide (30), which may reflect the same phenomenon.
The nature of the mechanism of response 3 could not be clarified in the present work. A reasonable possibility would have been some action of endogenous NO, because a previous investigation had revealed an important modulatory influence of NO on humorally induced vasoconstrictor tone in the kidney (8), and other observations had suggested a role of phasic changes in this dilator substance in dynamic autoregulation of RBF (27). However, clamping of the plasma levels of NO did not induce any alteration of the level of RVR during the plateau compared with furosemide alone.
In contrast, the time courses of RVR at least during the plateau phase were virtually superimposable after furosemide with and without the clamping of the plasma levels of NO. In addition, in a previous study (27) the clamping of plasma levels of NO by a very similar protocol indeed had an effect on the autoregulation of RBF. It should be noted that the present finding does not contradict a regulatory role for NO, operating in conjunction with the TGF (47) or mesangial chloride concentrations (46), because the present findings were made after blockade of the TGF by furosemide. In this respect, there is also no conflict with our previous finding of a phasic regulatory role of NO in RBF autoregulation (27). The present results rather suggest that the latter effect may be due to a TGF-associated mechanism.
Despite the small number of experiments and possibly confounding influences of kinins induced by the angiotensin-converting enzyme inhibitor, the experiments during clamping of ANG II plasma levels argue against ANG II as a mediator of the slow response of RVR. What the actual underlying causes are can only be speculated about. Possible factors include ATP, adenosine, or other purinergic derivatives (38), cytochrome P-450 metabolites (19), or intrarenally formed dopamine (33). Yet another possibility is that response 3 reflects a slow component of the myogenic response. Modifications in the kinetics of the myogenic response have been observed in the dependence of the rate of pressure change (15, 18) and after interference of the TGF (49).
Finally, the enhancement of response 1 after furosemide deserves some comment. It indicates an almost synchronous response of the whole preglomerular vasculature and also suggests that the dynamic properties of the myogenic response become altered in response to changes in the activity of the TGF. Changes in the kinetics of the myogenic response have also been reported from direct observations of afferent arterioles after elimination of the TGF by papillectomy (49). The fact that the augmentation of response 1 was even more pronounced after additional clamping of NO plasma levels is consistent with a role of shear stress-induced NO release for the reduction of resonance of the myogenic response (26).
Quantitative Considerations
During the period of pressure reduction, RVR fell by ∼50% of the baseline level, independently of whether the pressure reduction was prolonged for 5 min or changed to a complete occlusion. This indicates that half of the resting vascular tone is due to autoregulation and is thus available for regulatory vasodilatation. This is in good agreement with the view that the glomeruli are situated midway between pre- and postglomerular resistance and that the autoregulatory adaptation occurs predominantly in the preglomerular vessels (48), where it is brought about by all segments of this part of the renal vascular tree (9). It should be noted, however, that it cannot directly be inferred from the observation of the maximal vasodilatation in response to the pressure reduction well below the lower limit of autoregulation how efficiently this vasodilator capacity is employed for autoregulation within the autoregulatory pressure range. Therefore, the present results allow only conclusions regarding the total capacity of pressure-dependent vasodilatation from the basal vascular tone. In contrast to the autoregulatory efficiency (30), the vasodilator capacity was not significantly affected by furosemide in the present results.
Because the regulatory mechanisms operate at different velocities, their relative contribution to the total amount of this autoregulation can be estimated, because of the following reasoning. Immediately after the pressure reduction, all three mechanisms contribute their maximum vasodilator signal. Subsequently, the fastest response adapts its influence to a vasoconstrictor influence according to the new pressure, while the other two continue to provide a vasodilator signal. Therefore, during the plateau phase, the relative contribution of the myogenic response can be estimated from the rise in RVR. This seems to amount to 40% of the total response. After blockade of the TGF, only the myogenic response and response 3 are operative. Therefore, the initial constrictor signal of the myogenic response is opposed only by the vasodilator signal of the more slowly respondingresponse 3. Accordingly, the observations after furosemide suggest that, in the absence of the TGF, the myogenic response contributes 74% to the total autoregulatory effect, whereasresponse 3 provides the remaining 26%. Under the assumption that only the myogenic response, but not the third mechanism, is enhanced after furosemide, it may be argued that the TGF contributes the remaining 34%. Although this estimation must remain open, the assumption receives some support from the observation that the slope of RVR during the plateau phase was almost identical to that with and without furosemide. Because the step responses were investigated between 50 mmHg and resting arterial pressure, it is possible that this mechanism is active only in this low-pressure range. In this respect, it might be important to an understanding of ischemic acute renal failure. Whether and to what extent this mechanism also contributes to autoregulation at physiological arterial pressure levels cannot be decided from the present data and have to await further study.
Comparison With Hindlimb Vasculature
The observed response time in the range of 30 s is very similar to those observed by other authors in visualized arterioles in the hindlimb muscle of cats (25) and dogs (16,18) as well as in the cremaster muscle of rats (22,36). The direct comparison in the present study of the vascular responses in the renal and the hindlimb circulation in animals of the same strain (in 3 of them, also in the same individuals) clearly shows that there is a distinct difference in the time course of the myogenic response in these two vascular beds. Teleologically, this could provide protection for the capillaries from rapid increases in pressure, which might be more important in the kidney than in skeletal muscle. The same consideration might apply to the mesenteric vasculature, where the myogenic response also seems to be faster than in muscular tissue (1). The fast response of the renal vessels does not seem to be an invariable feature, because other response times, more closely resembling the pattern in skeletal muscle arterioles, have also been observed in renal vessels (17, 52). In one of these cases, embryonic renal tissue had been transplanted to the hamster cheek pouch, the native vessels of which usually respond more slowly than original renal arterioles (17). It is therefore conceivable that the time course of the myogenic response may also be under the influence of tissue-specific paracrine signals.
Our data show that, in addition to the myogenic response and TGF, a third regulatory mechanism significantly contributes to the autoregulation of RBF, which is independent of NO and probably also of ANG II. Although our data do not provide direct evidence that this mechanism also contributes to autoregulation when the TGF is intact, the observation of the slow rise in RVR during the plateau under control conditions, which displayed almost the same slope as that after furosemide, supports this conclusion.
All three mechanisms seem to contribute equally to basal resting tone of the renal vasculature. This raises the question of whether the relative contribution might be altered, particularly under conditions known to be associated with a modulation of the gain in TGF, such as changes in blood volume or the activity of the renin-angiotensin system (38).
Furthermore, the comparison to the hindlimb circulation demonstrates that the myogenic response is substantially faster in the kidney than in the skeletal muscle. This difference may be relevant for the local regulation of blood flow and capillary pressure as well as for the variability of systemic arterial pressure.
Finally, the present results demonstrate a remarkable capacity for pressure-dependent adaptation of vascular tone in the vessels of the hindlimb, which seems to even exceed that in the kidney. Although this does not allow direct conclusions about the autoregulatory efficiency, the finding raises the suspicion that autoregulation in the skeletal muscle circulation might be more efficient than presently believed (11). The estimation of the autoregulatory strength in this vascular bed, however, will remain difficult, as noted by Jones and Berne (25) with respect to the ample distribution of vasodilator fibers in this region, which are in frequent use in the conscious animal (29).
We thank I. Keller, L. Mahl, E. Röbel, and A. Klein for excellent technical help.
This study was supported by the German Research Foundation (Ki-151/5–3 and 5–4, and Graduiertenkolleg für Experimentelle Nieren-und Kreislaufforschung der Universität Heidelberg).
Address for reprint requests and other correspondence: A. Just, Dept. of Cell and Molecular Physiology, The Univ. of North Carolina at Chapel Hill, Medical Sciences Research Bldg. CB#7545, Chapel Hill, NC 27599-7545 (E-mail: just{at}med.unc.edu).
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 © 2001 the American Physiological Society


text:
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Showing 1 - 24 of 106 Women Hoodies

subset: commoncrawl


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He received a B.S. degree from Trinity University and holds Series 7, 9, 10, 24, 55 and 63 Licenses.
© 2017 Northern Trust Corporation. Head Office: 50 South La Salle Street, Chicago, Illinois 60603 U.S.A. Incorporated with limited liability in the U.S. Products and services provided by subsidiaries of Northern Trust Corporation may vary in different markets and are offered in accordance with local regulation. For legal and regulatory information about our offices and legal entities, visit northerntrust.com/disclosures.
This material is directed to professional clients only and is not intended for retail clients. For Asia-Pacific markets, it is directed to institutional investors, expert investors and professional investors only and should not be relied upon by retail investors.
SEC Rule 606 Report – 1st Qtr, 2016


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Reads: 331 | Likes: 0 | Shelves: 0 | Comments: 25
Miscellaneous by: angellynn
By: Angellynn
I have recieved eleven particiapants for this challenge. I needed at least 21, but oh well, we cant let that spoil our fun, now can we.
Now to refresh your memory on the rules...
When you entered this challenge, i ask you to give me a number. Now what you have to do is... At the end of this message, you will find your name, the number you gave me, and an icon.
When you have your icon, you are to start the hunt for it on one of my writings. It may take you awhile, and maybe not.. That depends on how well you are at finding things. This is all for fun, and i am by no means trying to increase my ratings.
After you have found your treasure ( Icon ). Come back to this page, and post where you found it, and the tile of the piece. That will determine your subject for the writing competition, get it!!!
Now doesn't this sound like fun!
Please! You do not have to comment, or read any of the pieces. Just scroll down to the end of the page. If the icon is'nt yours, go to the next one, etc etc etc!
I'm going to give you a hint... Their only under poetry. So forget about looking under myshort stories, and novels.
I have made a slight change in the rules. I will allow short stories, as some of you dont do poetry. So you have a choice to do a poem, poem/story, or short story. I'm flexable, and cant wait to see what you guys come up with. Good Luck!
VIPER- #4 ( I've been found )
FANCYJUMPER- #5 ( I've been found )
GADZOOKZIIE SPICE99- #7 ( I've been found )
MIKA- #10 ( I've been found! )
MATIUS- #12 ( I've been found )
STORMY RAINES- #13 ( I've been found )
SUNSHINE RAINES- #16 ( I've been found )
VAMPIREGIRL17- #17 ( I've been found )
BAZ- #19 ( I've been found! )
MSSJENN- #21 ( I've been found )
Manyfacets- # 11( I've been found )
Thats it! Start looking. If you need any help, or have any questions. Please let me know!
THANKS TO EVERYONE! GOOD LUCK! HAVE FUN! Angellynn :)
© Copyright 2017 angellynn. All rights reserved.
Add Your Comments:
Yay I found it! Its below "Love At First Bite". :) I didn't comment on any of your works, but I did skim through quite a few and I love them! :) So now you are going to give me a topic? I can't wait! :)
Your topic will of course be on the subject of vampires. Lol! I hope you like it. Now you are ready to write me a story/poem or short story on the subject of vampires.. Make it really interesting, i cant wait to read what you come up with! Let me know when you post, and please post it here. Its easier to keep up with that way. Congrats on finding it, and good luck writing...
Angellynn :D
Hi Angellynn. Found my icon once on "Darlyn Angel" and 39 times on "SECRETS". I assume you meant the former..?
Yes Darlyn Angel is correct. I dont know what happened with the secrets thing. Anyway, congrats on finding your treasure, you guys are quick! Now your subject will be Angels. It can be dark or spiritual. Its totally up to you, so long as it is about an angel(s). You are a wonderful writer, so this should be a breeze for you. Congrats on finding your treasure, and good luck writing. Short story or story/poem. Now get to work Baz. Lol!
Angellynn :D
FOND IT!!!! YAY!!!! on 'FAIRY SPRINKLES'
i found it faster than i thought i would lol because wow! you have lots of poems... i must say they are great! XD
Thats wonderful jenn. But just so you know. You didn't have to read them. Only scroll down and look for your treasure. But i appreciate your reading. Ok You found it on Fairy Spinkles. So you must write a story/poem or short story on Fairies, or a fairy. I saw all your comments, and almost fell out of my chair. Lol! Good Luck! Let me know when and what you have written. Thanks Alot! Happy Writing, and congrats on finding your treasure.
Angellynn :D
Thanks for letting me join in!! I have found my icon!
Its in the poem ; GOOD BYE TO YOU MY LOVE!!
Great GadzookziieSpice99! I hope you enjoyed the hunt. But the challenge is'nt over. I spelled your name wrong. I will correct it, i promise. Ok your subject will about saying goodbye to a loved one. It can be anyone of your choosing. A husband, boyfriend, ect.. It doesn't have to be death either. Just about ( Goodbye ). Good Luck Gad! I'm looking forward to reading what you come up with. Let me know, by posting it here. Easier to keep up with that way. Have Fun!
Angellynn :D
ohh i knew i didn't have to read but really like your poetry and couldn't stop myself lol ... oops i leave to many comments aww now i feel like an stalker.
i'll let you know when i have my writing ready! i'll try to make a poem, but i think a story is more possible from me
Take care
Aww you erased all my comments? mmm that makes me feel really bad. you didn't have to respond them but for same reason erasing them makes me feel really bad. sorry if it bothered you, i like to comment on the work i like, and like those poems.
No i didn't erase them. Booksie did that. I'm sorry, it wasn't intentional.. I've been having a lot of problems lately here on booksie. Theres no way i would do it deliberately. I lost three comments yesterday. I was trying to delete only one comment from someone trying to join the hunt. If i deleted yours, it was a mistake.. I'm sorry. It was a lot of trouble for you. I have e-mailed booksieguy, about this problem.
Hay Hay Hay I fount it on I Stand In Darkness. This is so cool can't wait to get started. S.R.
YAY!!! I found my icon thingy in "Mourning Is Over". I'm, also pretty sure that I found everyone else's icon too :P I can't wait to start, although I'll probably have to stay up late since I have a few major tests to study for and a short story challenge :P
Thats great Fancy! You found your treasure. Ok. Your subject is Mourning. It can be anyone, a parent, boyfriend, child, etc! Its a hard subject to write about, but i've read your work. I know you can do it. Good Luck! Let me know here on this page when your finished.. Thanks!
Angellynn :D
Hi angellynn. You are really killing me with these challenges! This was even harder than the last one!
Anyway, I have posted my entry "It Is Your Time" on my site. Its first ever short story, so don't expect too much. And I hope the subject is not too off-topic, but I really struggled with this one.
hay i found mine on My heart dont understand!
Ok I found mine on that thing you do.
I'm struggling with a little writer's block right now so I haven't written my piece yet. I'm not exactly mad about vampires either. But I'll stick to my topic. ^^ I just want to ask when our entries are due. =)
FOUND IT!!!!! It's in Light Of Darkness Right????!!?!! PLZ say I'm right!!! :P Haha, extremely hyper right now. :P Like seriously. HYPER. On life. And excitment. :P Ha-ha. :P I like smilies.:P ;P ;D :D XD :) :P
Thats great hon. I'm so happy for you. Yes you are correct. Congradulations on finding your treasure. Now i must give you a subject to write your story/poem or short story on. Since the piece contains light and darkness. You can write your piece on either of those subjects. Its up to you. If you really want a challenge. You write about both, its totally up to you.Please let me know right here when you are finished with your story, its so much easier for me to keep up with. Thank you, and have fun. there is no deadline as of yet.. So get to work my friend, and good luck!
Angellynn :D
Brenda your treasure is the maid smiley. When you have found your treasurew icon. Come back here with the poetry title, and i will give you your subject. Good luck, and happy hunting..
Angellynn :D
What a hunt! I went through the poetry twice,
I found one similar to what you assigned to me
but could not find an exact match...so I hope
I have it right.
Letter From My Soul is what I hope to be correct
I know that its taken a while to do it (booksie has been down for the hundreth time this month) my work is;
a poem called 'What hurts Most' I really hope you like it and it is true... maybe a little cheesy? Please leave some critisism is it needs it. Thankies Dannielle
Hello angellynn I have finally finished my short story for the challenge. Its called When The Lights Go Out.
I tell you what this was not an easy challenge wow thanks for giving my brain a once over lol. S.R.
I found it on the poem My Friend Teddy
More Other Miscellaneous
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Short Story / Gay and Lesbian
Book / Romance
Book / Humor
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Poem / Poetry


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Mon 30th Dec 2013 8:00amEscape Surfboards's Polzeath Surf Report
Polzeath 8.30: All gone crazy again today as the wind which has been very strong overnight has whipped the sea into a frenzy, it's worth coming and taking a look at the spectacle. Surfing is going to be off the cards down here as even though the wind should relent in strength and swing more westerly. High water will be this afternoon at 3.30 and the outlook for the rest of the holiday is windy followed by more windiness, so big waves to be ridden. Come and see me today from 10 to 1.00 and see all the boards we have which will get you in the slot. . For more information on anything surf or surfboard, please call 01208 863962 or email: email@example.com check out our Facebook page https://www.facebook.com/EscapeSurfboards
View the Polzeath Surf Report and Forecast. Escape Surfboards's Reports have received a total of 954210 views.
This report has received 489 views since 30/12/13.


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Saturday, Nov. 10, 2012 | 12:50 a.m.
The Las Vegas Wranglers' slump continued as their losing streak was extended to four games, following a 2-1 loss to the Alaska Aces on Friday at the Orleans Arena.
The Wranglers dropped to 3-5-0-1 and find themselves in last place in the Western Conference early in the season. The Aces, on the other hand, improved to 7-4-0-0, and are two points behind the Idaho Steelheads and Ontario Reign.
Nick Mazzolini scored two goals to lead the Aces.
Per the continuing trend with the Wranglers, the opposing team drew first blood in the first period.
Mazzolini scored a power-play goal at the 8:56 mark. Garry Nunn and Kane Lafranchise assisted on the goal.
Then 11 minutes into the second period, the Wranglers snapped 172 minutes of scoreless hockey when Eric Lampe scored to level the game at 1.
The score remained tied for close to eight minutes before Mazzolini scored his second goal of the night.
Alaska's Mark Guggenberger made 30 saves, while Las Vegas' Joe Fallon saved 35 of 37 shots.
The two teams wrap up a three-game set Saturday at the Orleans Arena.


text: | > dpkg-distaddfile dpkg-preconfigure dpkg-source | > dpkg-divert dpkg-reconfigure dpkg-split | ^^^^^^^^^^^^^^^^ | ??? Aaaaargh! Sometimes I wonder if I should give it all up and take up knitting instead. Many thanks for pointing that out. I'll read man mutt to deal with your cc comment; something I'm sure you'll appreciate!


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BikeSmarted - the end of the programme
29 August 2017
27 September 2016
If you commute a long distance to somewhere not served brilliantly by public transport, why not car-share to work? It vastly cuts the costs of commuting in a car by yourself, and is a viable way to helping cut emissions caused by regular car use. If half of UK motorists received a lift one day a week, congestion and pollution would be reduced by 10% and traffic jams by 20%!
Here are some tips to help you create a great car-sharing arrangement that'll help you keep saving costs and CO2e well into the future. Who knows, you might develop a great friendship too?
Who knows where car-sharing could lead and how much fun you could have...!


text:
- Suffield Academy08.Dec 2015
- Employee
Workplace Safety
Suggestions for improvement
- As I was in a temporary position I cannot speak to the way improvements could be made for full time employees, but my experience was great.
What I like about the company
I can honestly give it five stars in all those categories because not only was it a fun and pleasurable place to work but in the month I took over the art students while the regular teacher was on sick leave they gave me the freedom to create my own curriculum that was challenging for me as well as the students. The facilities were fantastic, the opportunities for creative exploration immense.


text: Big day tomorrow! I'm trading in my A4 S-Line 2.0 TDi; I've owned from new for 2 and a half years and it has been a fantastic car (my first Audi). I'm really going to miss it In its place, I'll be picking up a brand new A6 S-Line 2.0 TDi, I'm really excited about the new car; I hope the A6 will bring me as much pleasure as my beloved A4. Dave.


text:
Classic sailing yacht EUGENIA was designed by naval architect Philip Rhodes and built by San Germany yachts in 1968. The 22.11m (72.6ft) yacht has been meticulously maintained and is available for yacht charters for up to 7 guests in the East Mediterranean. S/Y EUGENIA has a professional crew of 3 to ensure a relaxing and memorable sailing vacation.
Crete, Athens, Adriatic Sea, Greece, East Med, Kos, Lefkas, Paros


text:
News BreaK Search:
Manchester United 4-1 West Ham United: Mkhitaryan, the playmaker
9 monthes ago - By Comcast SportsNet Baltimore
Jose Mourinho is within two rounds of the EFL Cup Trophy after Manchester United beat West Ham United on Wednesday.
Read more ...
The headlines of News BreaK
North Korea might test a hydrogen bomb in the Pacific Ocean
North Korea is interested in testing a hydrogen bomb in the middle of the Pacific, according to reports. The move would be in direct response to President Trump's latest threat...
North Korea's Kim: Trump 'will pay dearly' for comments at UN
In the statement, Kim says North Korea will make the US leader "pay dearly for his speech calling for totally destroying the DPRK."
Lawyer: Former Patriot Aaron Hernandez had 'severe case' of CTE
Jose Baez, the defense attorney who represented Aaron Hernandez during the former NFL star's second murder case, said a brain examination determined that the 27-year-old had a...
Facebook CEO to give Congress details on thousands of ads bought by a...
Facebook says CEO Mark Zuckerberg will provide to Congress the contents of 3,000 ads bought by a Russian agency.
Mexican officials: No girl trapped in collapsed school
A military official says there is evidence of a person who may be alive, but it is not the missing child that became a symbol of hope following the massive earthquake.
Ex-Trump adviser claims Steve Bannon co-wrote UN speech
Steve Bannon, the former chief strategist for President Trump, reportedly helped write the provocative address to the UN General Assembly this week in which Trump dubbed North...
Federal employees ordered to attend anti-leaking classes
The president and his administration have expressed anger over repeated leaks of information to media organizations in recent months.
Liliane Bettencourt, world's wealthiest woman, dies at 94
Liliane Bettencourt, the world's wealthiest woman and heiress to the L'Oréal cosmetics empire, has died at the age of 94.
Deaf, nonverbal man holding pipe fatally shot by Oklahoma City police officer
A neighbor said he yelled at officers that suspect was deaf.
What does Target's new wine taste like?
Find out if the $5 bottles are wine lover approved!


text:
Article List
ITC bans sale of Samsung products that infringe Apple patents
On Friday, the ITC made Apple Inc. very happy when it issued a ban on some Samsung Electronics Co. products that it found infringed on two Apple patents.
Marvel can keep rights to the Fantastic Four and other comic book characters
Marvel Entertainment won a smackdown at the 2nd Circuit on Thursday in its dispute with the children of comic book artist Jack Kirby
Schools cannot punish students for lewd speech with a political or social message
A 3rd Circuit ruling that seems silly at first actually reshapes how schools can regulate students' free speech.
SAC trader's lawyers seek access to witnesses
Former SAC Capital Advisors portfolio manager Michael Steinberg's lawyers are asking the court to grant them access to witnesses that the Securities and Exchange Commission has against him.
Apple displeased with DOJ e-book court order proposal
On Friday, the Department of Justice (DOJ) proposed a court order to regulate Apple's sale of e-books from now on, and Apple was not pleased with it.
California city sues Chevron over refinery fire
The city of Richmond, Calif. filed a lawsuit against Chevron Corp. on Friday, accusing it of willful negligence that led to last year's enormous refinery fire.
Roundup: 2nd, 4th, 5th and 6th Circuits
New R-3 100 program identifies rising in-house talent
We are proud to introduce the R-3 100 program—a list of 100 women who will likely be ready in three years to become general counsel. Hence, R-3 100—"ready" in "three" years.
Zynga sues over "Bang with Friends" app
The app "Bang with Friends" is pretty much what it sounds like.
Apple sued for searching store employees for stolen merchandise
Some former Apple store employees are claiming that the tech company owes them wages lost during the time they spent standing in line, waiting to be searched and prove they weren't trying to steal any store merchandise.


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We Love German Pinschers
Daveren Show News Flash
Welcome to my website! If you are looking to learn
more about German Pinschers you have come to
the right place! My website is packed full of
information & photos of German Pinschers. I am
an AKC Breeder of Merit, hobby breeder, show
ring exhibitor, and a huge fan of the fun fabulous
breed called the German Pinscher (GP for short)!
My goal is to preserve, promote, and look after
this breed for future generations to cherish &
I hope you enjoy my website & come back often!
-Jill Eastman
Daveren German Pinschers
2016 was another great year!!
Daveren finishes 2016 with the #1 German
Pinscher in the USA!
SILVER GCH CH Daveren's Life of the Party
Daveren wins BEST OF BREED at the 2016
Westminster Kennel Club Dog Show!
GCH CH Daveren's Life of the Party
Daveren wins BEST OF BREED at the 2016
AKC National Championship!
GCH CH Daveren's Life of the Party
Daveren finishes 2016 with 4 of the top 20
German Pinschers in the USA!
2016 brought 5 New Daveren Champions & 3
New Grand Champions!
Visit Our Show News Page for More Info!
More Daveren News .....
Nelson wins Best in National Specialty Show 2015!
Nelson's mother 'Pink' Award of Merit, 'Colbie' Select &
'Taylor' Best Bred-By
*Daveren German Pinschers are #1 in the USA!
for 2013, 2014, 2015, 2016, 2017
* Nelson - 2016 & 2017 #1 All Systems
*Pink - 2015 - #1 GP All Systems
*Tai - 2014 - #1 All Systems
*Meeka - 2014 - #1 GP Bitch All Breed System
*Tai - 2013 - #1 GP Breed System
Nelson is the #1 German Pinscher in the USA for 2016!
2016 & 2017
© Daveren German Pinschers - Albuquerque, New Mexico, USA - All Rights Reserved
This site it's contents may not be reproduced in any manner without written permission from the owner:
Jill Eastman - firstname.lastname@example.com
de with Xara
All Of Our Dogs
Our Boys
"Nelson" - BISS GCH CH Daveren's Life of the Party
"Atom" - CH Daveren's Atomic Love
"Liam" - GCH CH Daveren's William The Conqueror
"Parker" - GCH CH Oakwood V Kaitlers Tribute RA CAA CGC
"Cooper" - CH Daveren's Drops of Jupiter
Our Girls
"Pink" - GCH CH Daveren's Party Girl
"Meeka" - GCH CH Daveren's Tribute to an Amazing Dream
"Colbie" - GCH CH Daveren's Brighter than the Sun
"Summer" - CH Daveren's Midsummer Nights Dream
"Rose" - JCH Rus Legendorf Shantli Ros
"Daya" - GCH CH Daveren's Sit Still, Look Pretty
Our Foundation
"Devin" - CH Oakwoods Starlette
"Kylie" - GCH CH Angelsun Reisenable Dream
"Parker" - GCH CH Oakwood V Kaitlers Tribute CA CGC RN
"Markus" - Kaitler Mandrake
Our Retired Dogs
"Tripper" - CH Daveren's What A Trip CA
"Chase" - CH Daveren's Chasing Dreams RN
"Zeus" - Aust. CH Masterkarn Boyznblack
"Taz" - CH Legacy's Gold-en Nugget II
"Coral" - CH Daveren's Riptide
"Delu" - Daveren's Only You
"Amber" - GCH CH Daveren's Amber Sunset CA
"Tai" - GCHG CH Daveren's Peaceful Dream CAA CGC
"Claira-Bell" - CH Daveren's I Love Moo
Our Champions
In Memory


text:
Fraxel ruined my skin!!! It took away the fat and muscle in the lower part of my face. It left my skin very dry and old looking. I had beautiful skin before and was only doing it to stay young looking. I hate how I look now, 2 years after my last treatment. My doctor told me she was sorry that I had such bad results but did not have any answers for me. Do not do it, you will regret it!!! Lisa
Hated my Experience
Fraxel ruined my skin!!! It took away the fat and...
Was this review helpful? {{ voteCountOthers + ' other' + (voteCountOthers == 1 ? '' : 's') }} found this helpful


text:
Our product innovation and systems expertise in sensing, imaging and wireless connectively help you meet increasing design challenges and achieve the highest quality and reliability that the healthcare market demands.
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Design trends and innovative ideas to help you create the next coolest thing in medical and health technology.


text:
Good Stuff
So, I'm really happy about life. I really like Megan a lot now. And I want to tell her how I feel. Jeanne, thank you so much for helping me sort out my thoughts and practicing, lol. :) And, today at school I got asked to the prom by this really hot girl. So, that really boosted my spirits. I was like, "Wow, I am already going with Megan but I totally would have said yes. Thanks, you made me so happy." And I felt so bad because its really hard to put yourself out there like that and ask someone that you hardly know. But, yeah. So, I asked Megan online to the Prom on Friday. But, because that's such a stupid way of asking someone, I decided to really overdo it, :) . On Tuesday I made this huge poster and hung it up in her spanish room (after I found it in the trash after I initially hung it in the lunch room) and it said, "Tizzona, girl, you is be so fine- Malcolm" and it was really funny. And, Wednesday I wrote her a poem which went something like
Without you I'm incomplete
I need to go to sleep
My pen is dead
I think of you when I see bread
If I were Chinese I'd pick you rice
But, because I'm white, Casserole will have to suffice
If I were Black I'd get you some Gumbo
But, because I love Disney you'll be forced to watch Dumbo.
If I were French, for you I'd eat a snail
XxpoysndeathwishxX is the girl I want to nail
If I were Western I'd buy you a bloody steak
We'd be like American Gothic, I call "Guy holding rake"
You are the "Gona" to my "Ria"
The bloody veins in my eye
Oh, Miss Tashonta Jackson, won't you make me a lucky guy?
- Dan Quayle
"vote yes on 26"
HAHA, yeah. And, on the back I drew a centaur. And, on Thursday, I drew her a caricature of herself and framed it. It didn't look like her but it was still nice, and I gave her a skimpy dress and huge boobs. One of those small bodies huge heads kind of caricature. And, on Friday yesterday now, (I need to go to sleep), I decorated her locker with all these things, and I couldn't blow up the balloons so I just threw them in her locker, lol. Thanks, to her sister for giving me her combo, :) . Yeah, so I think I win the award for most stuff done to ask someone to Prom.
Haha, goodnight. :) -Mario~~


text: Children at Beth Tikvah-B'nai Jeshurun Preschool in Erdenheim celebrated Jewish Book Month on Dec. 10 by having stories read to them by area authors of children's books. Featured (from left) are Michelle Farbstein, bookfair chairperson; Dale Orman, author of The Mom Mom Book; and Dolores Goldich, author of I Saw an Ostrich in a Chair. BTBJ held its Jewish book fair from Dec. 7 to Dec. 23.


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Slide to see the images
AKC PUPPIES ~ 3 beautiful puppies full of champions born!!! Mom, Dana ?Pentastar?s Tahiti Sunset? is PRA cleared. She comes from a ?Breeder of Merit? Marian Dossinger. Dana is also CHAMPION SIRED by ?CH Pentastar?s Sunset Strip?. This hot beauty has 26 of 62 champions in her 5-year pedigree. Each of these puppies are beautiful with 3 girls born. Dad is ?Fuehne?s Hot Casanova?. He is a beautiful, gorgeous, top-notch show-quality deep red toy poodle with an excellent disposition. He is CHAMPION-SIRED by 5 lb apricot/red dad, ?CH Pentastar?s Sunset at Dossmar?. Champion dad has 7 of 15 champions in his 3-year pedigree!!! We have small children so every puppy has been socialized since birth to be around kids and being inside our home (and sleeping in their bed). These puppies are precious and ready for their new homes at 8 weeks old. Pictures updated weekly with weights for proper charting of their estimated adult weight. All shot records complete and a health guarantee provided. Puppies come with everything they need, their vaccinations (3 sets of wormings, 2 parvo vaccinations, 2 puppy shots, and a bordetella kennel cough vaccination). All puppies come with a blanket with mom?s scent on it, a 2-sided brush, a steel comb to fluff out their hair, and a toothbrush. You can see the difference in quality in our puppies! Additional pictures and parents can been seen on the website at www.fuehnefamilypets.com We live 30 min east of St. Louis off 64, can meet you at a convenient location. We travel often and are flexible in meeting you. Safe airline shipping also available for a flat cost of $350, inclusive on their airline flight, carrier, health certificate, and vet check. Call my cell at (618) 977-5177 See website for pictures, future litters, and prior owner testimonials!


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TEL AVIV (Jun. 12)
A farewell dinner was given here today to Dr. Jacques Faitlovitch, explorer and founder of the Jewish educational and welfare work among the Falashas, on the occasion of his return to Ethiopia to resume his work among the Jews there.
The activities of Dr. Faitlovitch will be financed by the American Pro-Falasha Committee which has been in existence for over twenty years. The committee, in 1923, established a Jewish school in Addis Ababa, capital of Ethiopia, where hundreds of Falashas were given a Jewish education. Soon after the Italians were driven out of Ethiopia last year, Dr. Faitlovitch re-established contact with the Jewish tribe there. Information which he received from them reveals that they suffered greatly under the Italian occupation.


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Hi all, Can anyone tell me if the bug reported on http://www.mail-archive.com/pgsql-bugs(at)postgresql(dot)org/msg07755.html is already fixed? I'm using PostgreSQL 7.3.3 on i386-pc-linux-gnu, compiled by GCC gcc (GCC) 3.3 (Debian), and I have the same problem described for 7.3.4 and 7.4.1. This bug can be reproduced creating a table, creating a view over the table and an insert rule over the view. The rule must be in the format: CREATE RULE "test_rule" AS ON INSERT TO "test" DO INSTEAD( INSERT INTO "test" (fld) VALUES (NEW.fld); ); If calling a function inside the rule's definition, the permission were read OK. SELECT my_func (NEW.fld) AS OK; Best regards, Luis Sousa
Next: From: SZŰCS Gábor Date: 2004-07-06 08:58:47 Subject: Immutable function in index Previous: From: Luke McFarlane Date: 2004-07-06 05:49:14 Subject: ecpg -D SYMBOL


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New Delhi, Aug 24: Responding to the Swiss Bank's rejection to disclose account details, the Union Finance Minister Pranab Mukherjee has said that Indian government will look into the matter and discuss the bank's rejection to disclose the details with authorities in banking sector.
Earlier, Swiss Bank told India not to coming 'fishing' for account details citing that Swiss law and even OECD's Model Tax Convention do not permit 'indiscriminate trawling through bank accounts in the hope of finding something interesting'.
"This means that India cannot simply throw its telephone book at Switzerland and ask if any of these people have a bank account here," a top official at Swiss Bankers Association was quoted as saying in a news agency report.
This comes only a week after the Swiss bank UBS AG agreed to hand over details of 4,450 secret accounts to the US's Internal Revenue Service.
And also it is to be noted that Swiss bank-client confidentiality has never been 100 per cent absolute. Sources suggest that Swiss legislators made provisions for flexibility during criminal investigations and also in civil cases.
OneIndia News


text: Nominated for seven Academy Awards including Best Picture and winner for Best Visual Effects, Babe is the timeless tale of a young orphaned piglet. Through his own sheer will and remarkable way with words, he overcomes the odds to become a pig of destiny. Babes enchanting adventure begins in Farmer Hoggetts barnyard. Under the care of Fly, the sheep dog, Babe figures hes a sheep dog too - and acts like it! But on a farm where outlandish antics and outrageous characters abound, you come to believe it yourself - and root for the polite little pig as he competes in the National Sheepdog Championships.Check stock and price


text:
Product description
Item No. 60893_1040759401
The Marco Tozzi Milly ankle boots are finished with a gold-tone buckle to give them a cool metallic edginess. The flattering cut hits right on the ankle perfect teamed with jeans.
- Upper: leather
- Lining: textile/synthetic
- Heel height: 7cm/2.8 inches
- Fastening: zip
- Fit: standard
This season's must have accessory - The Debenhams Credit Card
Apply now and enjoy an extra 10% off* for your first week
*T&Cs apply, credit provided by NewDay Ltd. Subject to status. 18+ only.
Delivery / Returns
Free Returns
Subject to exceptions, Debenhams is happy to exchange or refund your purchase within 28 days of delivery. Please check here for more details on our returns policy and exceptions.See more information


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words // Zack Schlemmer
BAIT officially unveils their third and final model of the BASICS Program Gel-Lyte III with ASICS. After the first two GL3 models of the BASICS program featured a strong military inspiration with the use of camo, the "Nippon Blues" Gel-Lyte III is inspired by the Japanese roots of ASICS and the Gel-Lyte III.
Via BAIT:
Switching directions from the first two military inspired designs, the BASICS Model-003 Nippon Blues is a step back to pay homage to Asics. Inspired by Japanese culture and tradition, the Nippon Blues utilizes an indigo kasuri textile imported from Japan to adorn the upper. Maintaining the functionality of the BASICS designs, a durable deep navy, nailhead suede reinforces the Gel-Lyte III to withstand the wear and tear of everyday use. The Asics form stripe has been modified for a clean simplistic design, alongside red accents to complete the Nippon Blues motif. Hickory Denim lines the footbed as a nod to exemplify the western influence and relationship Asics has with BAIT.
Online registration for your chance to purchase the Nippon Blues Gel-Lyte III is now available via BAIT. Along with the raffle for Model-003, you'll also have another chance to purchase the previous Model-001 Vanquish and Model-002 Guardian, or all three shoes together. Visit the BAIT website for full details on the online raffles.


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RCR and ECR Honor Dale Earnhardt at Daytona
DAYTONA BEACH, Fla. (February 11, 2011) - Richard Childress Racing and Earnhardt-Childress Racing Engines will pay tribute to the life and legacy of the legendary Dale Earnhardt throughout 2011 Speedweeks at Daytona International Speedway.
Commemorative No. 3 decals will adorn all eight of RCR's race cars, transporters and pit boxes. ECR employees will wear special ECR/No. 3 hats at the track throughout Speedweeks while RCR employees will wear special RCR/No. 3 hats February 18.
"All of us at RCR and ECR are honored to pay tribute to Dale on this 10th anniversary," said Richard Childress, president and CEO of Richard Childress Racing and Earnhardt-Childress Racing Engines. "His legacy is still felt every day at RCR, ECR and throughout the world. We hope all of Dale's fans appreciate this salute to their hero and ours."
The No. 29 Budweiser Chevrolet has been adorned with a small No. 3 decal since Kevin Harvick assumed the driving duties of RCR's former No. 3 Chevrolet in the second race of the 2001 NASCAR Sprint Cup Series season after Earnhardt's passing at Daytona on February 18, 2001.
-source: rcr


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It's the world's most famous lie.
And now it's in the dictionary.
Not "That dress in no way makes you resemble a rabid Christmas tree." Not "Of course I am not videotaping this." Not "I have read the service agreement." Not "I'm entirely confident that this will be an effective method of contraception as long as we pray together afterwards."
No: "LOL." Based on the number of times I have typed this phrase, you would think that I spent my life constantly convulsed with helpless laughter. But in fact, nothing could be farther from the truth. I make Whistler's Mother look like she was having a good time. I have all the effervescent charm and delight of a tray of baked goods in the rain. Sometimes I laugh, but only in a brusque chortle when I have been forced to acknowledge my own mortality.
So never, when I typed this initialism, have I in fact been laughing out loud. They say that people who refer to themselves as intellectuals are automatically committing a social crime – and, usually, an error. The same is true of LOL. If I were scrupulously honest about this, I would have to type things like "IANALATWDTOPITRAATTTFTIARHAMMDSTIAATTDALAYDBI" (I Am Not Actually Laughing As That Would Disturb The Other People In The Restroom And Alert Them To The Fact That I Am Reading Here Although Miss Manners Does Say That Is An Acceptable Thing To Do As Long As You Don't Broadcast It" or "IWLBTIFBIWJATTACKEDBYABEAR" I Would Laugh Because That Is Funny But I Was Just ATTACKED BY A BEAR" or, as the site Unprovoked Digression suggests, "'iptychtsoemostwitbfaiwbabsaiidsitiwfsijsiwftayamt-wsiabsamwcftwiahputpamoabbabbpabwalltrtsmbeinluthftssoDcbffun' — 'I perceive that your communication has the structural or expressive markers of something that was intended to be funny and it would be a bit socially awkward if I don't say I think it was funny so I'll just say it was funny to appease you and make the whole social interaction a bit smoother and maybe we can forget the whole incident and hopefully pick up the pieces and move on, a bit battered and bruised but perhaps a bit wiser and less likely to repeat the same mistake but even if not let us take heart for the sweet salve of Death cannot be far from us now."
But after the Oxford English Dictionary decided to add "LOL" to its arsenal, I decided it was time to take a stand. The movement for Honest Abbreviations, Honest Acronyms starts here – or, as I like to call it, "HA, HA." Swing on over to my Facebook page and join us!
This is not a new idea or a novel objection. Many of us had already awakened to the innate mendacity of LOL and attempted to mend our ways by jumping onto the "Ha" bandwagon. Text or type something funny to us, and we'll respond with some elaborately calibrated assortment of "ha's." "Three or more ha's if I really laughed," we'll explain. "One sounds sarcastic. Two sounds like you didn't really laugh. Sometimes I shake it up by prefacing with "BAHA or "HOHOHA" to add a random, real-world element."
But this takes far too much effort! I used to read. Now I have to spend all that time calibrating my ha's. That was why LOL – or its less demure cousins, LMAO and ROFL – was coined in the first place. It was great when we actually were laughing. But then it grew into a form of courtesy. Now, in response to anything anyone types that seems remotely droll, we politely type "LOL" or "ROFL" into the keyboard to indicate that we are experiencing the mirth expected. It's worse than merely the online equivalent of the mirthless giggle, the polite laugh, the Professional Smile. The omnipresence of those leaves intact our ability to recognize a real titter or a genuine grin. But our watered-down online ha's and LOL's and ROFLMAO's are making it literally impossible to tell the true laugh from its phony counterpart. And that's an awful shame. We lose so much by communicating online – for instance, the ability to pick up on rich non-verbal cues that is the only thing separating us from the chat-bots who like to congratulate us on our weight loss. Must laughter be one of them?
So it's time for HA, HA. Please, I beg you, do not type LOL unless you are literally splitting a gut with actual mirth. Otherwise, pick an acronym that more accurately reflects the truth, like ISWYDT (I See What You Did There) or IATHOT (I Acknowledge The Humor Of That), or TRFA (That's Rather Funny Actually).
Maybe it'll wind up in the OED!


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By Karl B. Hille and Kelsi Loos
COLLEGE PARK – It wasn't bad investments or even an emergency that pushed Dennis and Stephanie Bradshaw close to a credit default. It was simply having a baby.
When the Bradshaws brought their second son home to Gaithersburg in July, 2010, $4,000 of the $10,000 hospital bill was not covered by his insurance. The family set up monthly payments with the hospital, and soon began using credit cards to cover other expenses.
Credit Debt Puts Families on Edge
Jason Flanagan went deep into credit card debt to support his wife and two daughters. He blames his divorce on struggles with money. Read More…
Dennis and Stephanie Bradshaw of Gaithersburg took on a hefty hospital bill when they brought home their second son in July 2010. And while credit cards served as a quick fix, they couldn't pay down their growing credit card debt without help from family.Read More…
"Obviously, I was charging for diapers, which was a huge expense," Dennis Bradshaw said.
The family kept charging food, gas, rent and other necessities until last April, when Dennis Bradshaw was paying more than $1,000 a month on five different cards at interests rates of 6 to 17.1 percent.
They cut back on expenses — Target brand instead of Pampers and bag lunches instead of McDonalds — but it wasn't enough.
To make ends meet, Stephanie Bradshaw asked her grandmother for help, and she gave them a cash gift. Dennis Bradshaw's mother also helped out with a series of cash gifts. His tax return went straight to the credit cards too.
He said he should be able to pay off his Bank of America card soon. But without a bare-bones budget and the generosity of relatives, the Bradshaws could easily have fallen into a cycle of default that has ensnared many.
Basic costs like housing, day care, transportation and medical needs rose twice as fast as wages in Maryland over the past decade. Many families have used credit cards to bridge the gap — even at the expense of paying the mortgage.
Unable or reluctant to seek government financial assistance, families are turning to credit as their safety net, state officials and advocacy groups say. As a credit card becomes more crucial to getting by, credit-card debt is taking the place of mortgage payments as a top priority for repayment.
"Credit cards are no longer being used for just discretionary purposes. People need their credit cards to buy gas, to function and go to work," said Mark Kaufman, commissioner of the Maryland Division of Financial Regulation.
The credit card has become such a survival tool, and mortgages have become such a losing investment for a broad portion of homeowners, that plastic has achieved new importance and priority in people's day to day lives, Kaufman said.
"Usually you pay your mortgage debt at the expense of their consumer debt. Now people are paying their credit card before they pay their mortgage," Kaufman said. "As home values deteriorate, you have less incentive to keep paying on that."
Credit-reporting agency TransUnion verified Kaufman's claim. Last year, Maryland ranked near the high end of mortgage delinquency – with more than 7 percent of loans in default by the end of 2011's fourth quarter. On the other hand, the agency reported that credit-card defaults fell even while credit-card debt continued to rise, leading some to conjecture that people are more careful to pay down their debt as the card becomes more important to getting by.
The Federal Reserve Bank of New York Consumer Credit Panel reported in 2010, that people may use their credit accounts to "smooth their consumption" in the event of a job loss, leading to more borrowing.
Marylanders racked up some of the highest rates of credit-card debt per capita, according to a 2008 study by the Corporation for Enterprise Development, a nonprofit think tank.
The average Maryland borrower owed $13,145 on credit cards at the end of 2011, including retail cards and other lines of credit. About 5 percent of borrowers were 90 days or more past due on their payments, according to the study.
Government assistance programs could help some to bridge the gap between wages and costs, but many working families make too much to qualify. The state saw a 43 percent increase in people seeking help from its Temporary Cash Assistance program between 2008 and 2012, but two-thirds were turned away as ineligible.
Others may be uncomfortable asking for help, state officials say. Instead they charge the difference between their salary and their costs.
"People are embarrassed. The last thing in their comfort zone is going to their neighbor and asking 'How do you get public assistance?,'" said Ian Patrick Hines, the communication director for Maryland's Department of Human Resources.
Medical Debt
Robin McKinney, director of the Maryland CASH Campaign, an organization that promotes financial stability for low-income families, said her clients have become much more likely to charge medical bills as they lose insurance coverage at work, lose their jobs, or start their own businesses.
"We see a lot of credit card debt that's really medical debt. People need credit and they need it now. When an emergency happens… they don't have enough money they have to pay for it," said McKinney.
Borrowers without insurance will pay their bills on credit, then suffer the effects of stress caused by dealing with those debts. "It's the spiral effect," said Sarah Johnson, director of the Baltimore CASH campaign.
Dennis Bradshaw had insurance through his account managing job at a high-volume printing company, but coverage was cut back through that plan because of rising health-care costs, he said.
While he could rely on family and save his way out of debt, people with long term-medical conditions or disabilities can't always work their way out of medical debt, as the expenses keep piling on.
A 2008 survey of low and middle-income households by the Access Project, a Boston-based nonprofit that aims to improve health-care access, found that half of medically indebted families used credit cards to pay for basic living expenses in the past year because they did not have enough money in their savings. Only one in five people without medical debt did so.
Families with medical debt owed an average of $2,194 on credit related to medical expenses.
Defaults: The Vicious Spiral
Consumer advocates warn that this tendency to rely on credit for basic needs could lead to late payments or defaults, subjecting the borrower to higher interest and more fees.
"The bottom line is that time is of the essence if a person is facing mounting debt," McKinney said.
Jason Flanagan, 31, learned that lesson the hard way. He began depending heavily on his credit cards in 2005 and 2006. The plastic helped him catch up from week to week as he juggled multiple jobs, college classes and a growing family with one young daughter and a second on the way.
"We'd use it to pay a bill, or — I was going to school at the time — I'd use it for school stuff," said Flanagan, 31, of Greenbelt. "We never used it for cruises or fancy vacations or big screen TVs. We just used it to pay bills."
Flanagan said he defaulted on two credit cards before he could finish his degree, and the financial pressure was part of the reason for his divorce.
His credit history limits Flanagan's options. He cannot buy a home or move to a bigger apartment to accommodate his two daughters when they come to visit every other weekend.
Learning to get by without credit has forced some financial discipline on him. Yet despite his credit card history, he said he still gets offers in the mail. Not as much as before the recession, the offers he does get are for subprime credit cards — those with interest rates around 24 percent.
More than half of Marylanders have taken such offers, said the CASH Campaign's McKinney. With high interest rates, it becomes harder and harder to pay down debt and mounting fees.
"Creditors aren't going to go away. Interest and fees will accrue. Collection activity will worsen and often times people find themselves in a deep hole very quickly," said Deanna Booker of the Consumer Credit Counseling Service, a financial education nonprofit group. "The idea is to start working on digging out of the hole as quickly as possible."


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Last season on "True Blood," somebody with a grudge against Bill Compton (Stephen Moyer) and Eric Northman (Alexander Skarsgard) may have been behind the release of Russell Edgington (Dennis O'Hare); the crazed Vampire King who vowed vengeance against them and their mutual lover, Sookie Stackhouse (Anna Paquin).
While "True Blood" won't return for its fifth season until June, HBO has released a behind-the-scenes glimpse of a preview scene in which the werewolf Alcide (Joe Manganiello) visits Sookie and gives her the bad news about Edgington's return before offering to protect her. However, Sookie's friend, Lafayette (Nelsan Ellis) is definitely not welcoming Alcide's assistance.
Fair warning, the language in this clip is very NSFW, so if you're in an office or around kids, turn down the volume.
We may infer from this scene that Lafayette is possibly the mysterious man (glimpsed in the season five teaser trailer) helping Sookie to bury the bodies of her friend, Tara Thornton (Rutina Wesley) and her murderer, Debbie Pelt (Brit Morgan); whom Sookie killed in revenge. They must have done a good job of cleaning up too, because Alcide doesn't seem to be aware that his former lover Debbie died in that room hours earlier.
"True Blood" season 5 will kick off on Sunday, June 10 only on HBO!
Share your thoughts and theories about the "True Blood" preview scene in the comment section below!


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Twin brothers, 80, die together from carbon monoxide poisoning
12:57 pm, Monday, February 24, 2014
Twin 80-year-old brothers died Sunday night from apparent carbon monoxide poisoning, Lewis County Sheriff's Officials said.
The brothers were working on the exhaust manifold of an antique car in the closed garage at one of the men's Chehalis home, deputies said. The other brother was visiting from Rainier.
When the wife of one of the victims returned home from a neighbor's home, she discovered the two men unconscious in the garage and called 911.
Medics arrived to find high levels of carbon monoxide in the garage and rushed both victims to area hospitals. One brother was taken to Centralia Providence Hospital where he was later pronounced dead. He was identified by the Lewis County coroner as William Schofield.
The other brother, Walter Schofield, was taken to Harborview Medical Center in Seattle where he later died Monday morning.
"These brothers were simply working on a car together and ended up dying from a silent killer," Lewis County Sheriff Steve Mansfield said in a statement. "Educate yourself about the dangers of carbon monoxide poisoning and keep you, your friends and family safe."


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Sunset Rock (TRAD)
Sunset Rock, tucked into into a northwest facing bluff on Lookout Mountain, is the grandmother of traditional climbing in the Southeastern U.S.
A part of Lookout Mountain Battlefield in Chickamauga and Chattanooga National Military Park, it is highly respected and protected by the local climbing community and the National Park Service as place of historical significance.
Because of it's northwestern facing cliff, Sunset offers a cool, shady place to climb during the spring summer and fall, but in winter can get a bit brisk.
To protect access for climbers and also the mountain's historical inegrity, please respect and obey all of the NPS climbing regulations for Sunset Rock.
The best place to park is Lookout Mountain Battlefield's Cravens House.
Southeastern Climbers Coalition Sunset Rock Information
Roots Rated Sunset Rock Information
Activity type
Traditional "TRAD" climbing with some set top rope anchors. DO NOT ANCHOR TO TREES. No sport climbing anchors.
Related Activities
Day hiking, trail running
Distance from Outdoor Chattanooga to Craven's House Parking Area
7.5 miles | 17 minutes
GPS Coordinates (Cravens House Parking Lot)
35.013496, -85.341629
Dates | Hours
6 a.m. Eastern Time to sunset. Strictly enforced.
Number Of Routes
100+ Some routes are permanently closed to climbing.
In Case of Emergency
Dial 911
Point Park Visitor Center (423) 821-7786
No. Nearest camping is at Cloudland Canyon State Park or Raccoon Mtn. Caverns and Campground
Contact Informaton
Chickamauga and Chattanooga National Military Park
Lookout Mountain Battlefield
Point Park Visitors Center
(423) 821-7786