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Generation and functional significance of CXC chemokines for neutrophil-induced liver injury during endotoxemia. Am J Physiol Gastrointest Liver Physiol 288: G880–G886, 2005. First published December 2, 2004;.—The hypothesis that the neutrophil chemoattractant CXC chemokines KC and macrophage inflammatory protein-2 (MIP-2) are involved in neutrophil transmigration and liver injury was tested in C3Heb/FeJ mice treated with galactosamine (Gal, 700 mg/kg), endotoxin (ET, 100 μg/kg), or Gal + ET (Gal/ET). Hepatic KC and MIP-2 mRNA levels and plasma CXC chemokine concentrations were dramatically increased 1.5 h after Gal/ET or ET alone and gradually declined up to 7 h. Murine recombinant cytokines (TNF-α, IL-1α, and IL-1β), but not Gal/ET, induced CXC chemokine formation in the ET-resistant C3H/HeJ strain. To assess the functional importance of KC and MIP-2, C3Heb/FeJ mice were treated with Gal/ET and control IgG or a combination of anti-KC and anti-MIP-2 antibodies. Anti-CXC chemokine antibodies did not attenuate hepatocellular apoptosis, sinusoidal neutrophil sequestration and extravasation, or liver injury at 7 h. Furthermore, there was no difference in liver injury between BALB/cJ wild-type and CXC receptor-2 gene knockout (CXCR2−/−) mice treated with Gal/ET. The higher neutrophil count in livers of CXCR2−/− than in wild-type mice after Gal/ET was caused by the elevated number of neutrophils located in sinusoids of untreated CXCR2−/− animals. The pancaspase inhibitor Z-Val-Ala-Asp-fluoromethylketone eliminated Gal/ET-induced apoptosis and neutrophil extravasation and injury but not CXC chemokine formation. Thus Gal/ET induced massive, cytokine-dependent CXC chemokine formation in the liver. However, neutrophil extravasation and injury occurred in response to apoptotic cell injury at 6–7 h and was independent of CXC chemokine formation.
- inflammatory liver injury
- neutrophil cytotoxicity
- apoptosis
- caspases
- CXC receptor 2
polymorphonuclear leukocytes (neutrophils) contribute to liver injury in a number of disease states, including hepatic ischemia-reperfusion (26, 28), endotoxemia (19, 29), sepsis (43), alcoholic hepatitis (2), remote organ injury (20,22), hemorrhagic shock (52), obstructive cholestasis (15, 18), and certain drug-induced liver injuries (8). The basic mechanism of a neutrophil-mediated pathophysiology in the liver requires the accumulation of primed and activated neutrophils in vascular beds of the liver, extravasation into the parenchyma, and the adherence-dependent cytotoxicity against hepatocytes (31). Neutrophils can accumulate in portal venules, sinusoids, and postsinusoidal venules (4, 12, 14, 18, 34, 53, 54, 56) and extravasate from all these locations (15, 18, 34, 54). However, extravasation from sinusoids is most critical for liver injury (6, 18). Blocking strategies directed against β2-integrins (15, 26, 29) and intercellular adhesion molecule-1 (11, 18), which eliminated neutrophil extravasation, proved to be highly effective in preventing neutrophil cytotoxicity in the liver. However, the chemotactic signal responsible for neutrophil extravasation has not been conclusively identified in any model.
Chemokines are a class of chemotactic agents with a relatively high specificity for individual leukocytes (40). α-Chemokines are characterized by a structural feature where the first two cysteine residues are separated by one amino acid (CXC). The members of a subgroup of this family, which contains the amino acid sequence glutamic acid-leucine-arginine (ELR), are chemoattractants for neutrophils (40). In the mouse, the most prominent ELR+ CXC chemokines expressed in the liver are the chemokine KC and macrophage inflammatory protein-2 (MIP-2) (47), which bind to the CXC receptor 2 (CXCR2) (3, 36). Although CXC chemokines are less potent activators of neutrophils than are cytokines and complement factors (1), excessive CXC chemokine formation in parenchymal cells can recruit neutrophils into the liver vasculature (13, 41,50, 58), induce transmigration, and cause injury (41). The most convincing evidence for the importance of CXC chemokines under pathophysiological conditions was provided in hepatic ischemia-reperfusion injury (23, 45). Neutralizing CXC chemokines attenuated hepatic neutrophil recruitment and the neutrophil-mediated injury phase in rat and mouse models of warm ischemia-reperfusion (7, 21,33, 38). On the other hand, in a model of α-naphthylisothiocyanate (ANIT)-induced liver injury, which involves injury by neutrophils (8), neutralizing CXC chemokines had no effect on neutrophil recruitment or injury (57). Thus the importance of CXC chemokines as a neutrophil chemoattractant and the exact mechanism may vary between different pathophysiological situations. We previously demonstrated that CXC chemokines are unlikely to be involved in neutrophil activation and recruitment into the hepatic vasculature during endotoxemia (1). However, we showed that parenchymal apoptosis is a critical event triggering neutrophil extravasation (30, 35). Because hepatocytes undergoing apoptosis can generate CXC chemokines (13), we tested the hypothesis that CXC chemokines formed by healthy or apoptotic hepatocytes might represent the signal for neutrophil extravasation and attack on hepatocytes in the galactosamine/endotoxin (Gal/ET) model of liver injury.
Male C3Heb/FeJ and C3H/HeJ mice (20–25 g body wt) or wild-type (BALB/c) and CXCR2−/− mice (BALB/c background) were obtained from Jackson Laboratories (Bar Harbor, ME). The animals had free access to food (certified rodent diet 5002C, PMI Feeds, Richmond, IN) and water. The experimental protocols were approved by the University of Arkansas and the University of Arizona. Animals were treated with Salmonella abortus equi endotoxin (ET, 100 μg/kg), galactosamine (Gal, 700 mg/kg), or Gal + ET (Gal/ET; Sigma, St. Louis, MO). Some of the animals were treated intravenously with anti-KC (5 mg/kg) and anti-MIP-2 (5 mg/kg) antibodies (R & D Systems, Minneapolis, MN) or nonimmune murine IgG (10 mg/kg; PharMingen, San Diego, CA) as described elsewhere (13). Other animals were treated intravenously with murine recombinant TNF-α, IL-1α, or IL-1β (2 μg/kg each; all from Endogen, Woburn, MA). Groups of animals were killed 1 or 3 h after injection of an inflammatory mediator or 0.5–7 h after Gal/ET or ET. Blood was collected from the vena cava into a heparinized syringe for analysis of alanine transaminase (ALT) activities and chemokine levels. Sections of the liver were fixed in phosphate-buffered formalin for histological analysis or frozen in liquid nitrogen.
To assess liver cell injury, ALT activities were measured in plasma by means of a kinetic test kit (catalog no. 68-B, Biotron Diagnostics, Hernet, CA). Plasma levels of MIP-2 and KC were measured with the respective ELISA kits (R & D Systems) according to the manufacturer's instructions. Caspase-3 activities were determined as described in detail elsewhere (30) with some modifications (16, 17). Briefly, liver samples were homogenized in 25 mM HEPES buffer (pH 7.5) containing 5 mM EDTA, 2 mM DTT, and 0.1% CHAPS. The homogenized samples were centrifuged at 14,000 g, and the diluted supernatant was assayed for the Z-Val-Ala-Asp-fluoromethylketone (Z-VAD-fmk)-inhibitable portion of the caspase activity with use of the synthetic fluorogenic caspase-3 (CPP32) substrate acetyl-Asp-Glu-Val-Asp-4-methylcoumaryl-7-amide (Peptide Institute, Osaka, Japan) at 50 μM. The samples were assayed in duplicate wells, with or without 10 μM Z-VAD-fmk, and the kinetics of the proteolytic cleavage of the substrate were monitored in a fluorescence microplate reader (Spectromax Gemini EM, Molecular Devices, Sunnyvale, CA) with 360-nm excitation and 460-nm emission wavelengths. Caspase-3 activity was calculated from the slope of the recorder trace and expressed as change in fluorescence per minute per milligram of protein. Protein concentrations in the supernatant were assayed using the bicinchoninic acid kit (Sigma).
Formalin-fixed portions of the liver were embedded in paraffin, and 5-μm sections were cut. Sections of the livers were stained for terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay as described in the manufacturer's instructions (Roche Molecular Biochemicals, Indianapolis, IN). The number of apoptotic hepatocytes was quantified in these sections on the basis of positive TUNEL staining and morphological criteria, as described previously (16, 17). The AS-D chloroacetate esterase technique was used to stain neutrophils in liver sections, as described in detail previously (27). Neutrophils were identified by positive staining and morphology and were counted in 20 high-power fields (×400) with a Nikon Labophot microscope. Only neutrophils within sinusoids or extravasated into the tissue were counted; the small numbers of neutrophils marginated within large vessels, e.g., hepatic venules, were not included, because they are not involved in the injury (6). Cell damage was evaluated in parallel sections stained with hematoxylin and eosin. The percentage of necrosis was estimated by evaluating the number of microscopic fields with necrosis compared with the entire histological section. The pathologist (A. Farhood) performing the histological evaluation was blinded with regard to the treatment of animals.
Ribonuclease protection assay.
All protocols followed the instructions for the RiboQuant Multi-Probe RNase Protection Assay System (PharMingen). The In Vitro Transcription Kit and a customized template set (containing mouse MIP-2, mouse KC, and L32) were used to synthesize a radiolabeled probe set using [α-32P]UTP. These probes were hybridized with total RNA isolated from liver tissue for 16 h. After digestion of nonhybridized RNA with RNase, the protected probes were separated on a denaturing acrylamide gel. The gel was dried and then exposed to X-ray film (Kodak X-OMat, Fisher Scientific, Pittsburgh, PA) for 12 h at −80°C. The developed X-ray films were scanned using a calibrated imaging densitometer (model GS-710, Bio-Rad Laboratories, Hercules, CA) and Quantity-One software (Bio-Rad).
Values are means ± SE. Comparisons between multiple groups were performed with one-way ANOVA followed by Bonferroni's t-test. P < 0.05 was considered significant.
CXC chemokine formation during endotoxemia.
To assess CXC chemokine formation during endotoxemia, plasma levels of KC and MIP-2 were measured by ELISA. ET or Gal/ET resulted in a rapid increase in plasma levels of KC and MIP-2 (Fig. 1). Peak levels of 2,000–2,500% (KC) and 3,600–4,000% (MIP-2) of baseline were reached 1.5 h after ET injection and then gradually declined over the next 4–5 h. Although drastically reduced compared with peak levels, plasma concentrations of KC and MIP-2 were still significantly above baseline at 6 and 7 h (Fig. 1). There was no significant difference in chemokine plasma levels between ET and Gal/ET at any time. On the other hand, Gal alone had no effect on CXC formation (Fig. 1). To verify that the CXC chemokines were formed in the liver, KC and MIP-2 mRNA levels were measured in the tissue with an RNase protection assay (Fig. 2). Similar to the time course of plasma protein levels, KC and MIP-2 mRNA levels were highest 1.5 h after Gal/ET (Fig. 2) and ET (data not shown) and then gradually declined. Again, the 6-h values were still significantly elevated compared with controls (Fig. 2).
Cytokines as inducers of CXC chemokine formation in vivo.
To evaluate whether cytokines are actually responsible for KC and MIP-2 formation during endotoxemia, ET-resistant (C3H/HeJ) mice were treated with Gal/ET. C3H/HeJ mice have a Toll-like receptor-4 deficiency (46) and, therefore, are unable to produce any cytokines in response to ET or Gal/ET in vivo (11). Gal/ET did not cause a significant increase of plasma KC or MIP-2 levels (data not shown), suggesting that CXC chemokine formation during endotoxemia in vivo is largely dependent on the production of cytokines. To confirm the role of cytokines as inducer of CXC chemokine formation in vivo, C3H/HeJ mice were injected intravenously with TNF-α, IL-1α, or IL-1β (2 μg/kg each). In general, all three cytokines proved to be potent inducers of KC and MIP-2 (Fig. 3). However, some clear differences emerged between these cytokines. Substantially higher and more sustained plasma levels of KC or MIP-2 were induced by IL-1α than by IL-1β or TNF-α (Fig. 3).
Pathophysiological relevance of CXC chemokine formation during endotoxemia.
To investigate a potential role of KC and MIP-2 in the pathophysiology of Gal/ET-induced liver injury, animals were treated with combined antibodies of KC and MIP-2. Gal/ET caused apoptosis, as indicated by the >20-fold increase in caspase-3 activities in the liver (Fig. 4). In addition, elevated plasma ALT activities were observed together with histological evidence of hepatocellular necrosis at 7 h (Fig. 5). The overall injury in this model is initiated by TNF-mediated apoptosis, which triggers neutrophil extravasation and neutrophil-mediated injury (30, 35). Consistent with this hypothesis, large numbers of neutrophils were present in the liver 7 h after Gal/ET; ∼35% of the total hepatic neutrophils were located in the parenchyma (Fig. 6). Treatment with control IgG or the combined anti-KC and anti-MIP-2 antibodies did not attenuate any injury parameter, including caspase-3 activities (apoptosis; Fig. 4), plasma ALT, and histological assessment of necrosis (Fig. 5). Furthermore, the antibodies had no effect on Gal/ET-induced hepatic neutrophil accumulation or extravasation into the parenchyma (Fig. 6). Because previous reports suggested that hepatocytes undergoing apoptosis can produce CXC chemokines (9, 13), we treated animals with the pancaspase inhibitor Z-VAD-fmk (10 mg/kg) 3 and 4.5 h after Gal/ET and measured CXC chemokine formation at 5.5 h. These doses of Z-VAD-fmk and other pancaspase inhibitors are known to eliminate apoptosis in the Gal/ET model and prevent extravasation of neutrophils (17, 25, 30). Consistent with previous observations, Z-VAD-fmk attenuated the increase of caspase-3 activities by 92% and the number of TUNEL-positive hepatocytes by 87% (Fig. 7). However, Z-VAD-fmk treatment had no significant effect on KC or MIP-2 formation, despite its profound effect on apoptosis.
Gal/ET-induced liver injury in CXCR2−/− mice.
Although the doses of anti-KC and anti-MIP-2 antibodies used in this study were effective in reducing hepatic neutrophil accumulation in the Fas receptor-induced apoptosis model (13), we wanted to confirm our findings with a different approach. Therefore, we tested the susceptibility of CXCR2−/− mice to Gal/ET-induced injury. CXCR2 is the only receptor for CXC chemokines in mice and is used by KC and MIP-2 (3, 36, 44). Wild-type BALB/c and CXCR2−/− control animals had normal levels of plasma ALT activities, no necrosis, and baseline levels of hepatic caspase-3 activities (Table 1). Untreated CXCR2−/− mice showed significantly elevated numbers of neutrophils in the liver, all of which were located in sinusoids (Table 1). Similar to C3Heb/FeJ mice, Gal/ET-induced hepatic neutrophil sequestration and extravasation resulted in severe liver injury in wild-type BALB/c mice at 6.5 h (Table 1). However, all parameters of cell injury were similar in CXCR2−/− and wild-type animals (Table 1). The overall numbers of neutrophils in the liver as well as the numbers of extravasated neutrophils were higher in CXCR2−/− mice. However, the percentage of extravasated cells was similar in wild-type (42 ± 4%) and CXCR2−/− mice (39 ± 6%).
ET-induced CXC chemokine formation.
The objective of this investigation was to determine CXC chemokine formation and assess its pathophysiological relevance in the Gal/ET model of apoptosis and inflammatory liver injury. Measurement of plasma chemokine protein levels demonstrated a massive formation of KC and MIP-2 in response to Gal/ET and ET but not Gal alone. These chemokines were at least in part generated within the liver, as indicated by the parallel rapid increase and gradual decline of hepatic mRNA levels and the plasma KC and MIP-2 protein levels. However, it cannot be excluded that other, extrahepatic sources also contributed to CXC chemokine concentrations in plasma. The increase in KC and MIP-2 mRNA within the liver developed parallel to enhanced TNF-α formation during endotoxemia in C3Heb/FeJ mice (55). On the other hand, Toll-like receptor-4-deficient C3H/HeJ mice, which are unable to generate cytokines in response to Gal/ET in vivo (11), did not produce chemokines during endotoxemia. However, injection of murine recombinant TNF-α resulted in a rapid CXC chemokine formation in the liver. On the basis of these data, it can be concluded that CXC chemokine formation after ET is almost entirely cytokine dependent. This does not involve only TNF-α but most likely also IL-1. The delayed decline of CXC chemokine mRNA and plasma protein levels compared with TNF-α suggests that IL-1 might be involved in maintaining CXC chemokine levels after TNF-α formation has stopped. Indeed, IL-1α and IL-1β are also potent inducers of KC and MIP-2 formation.
Pathophysiological relevance of CXC chemokine formation.
CXC chemokines are potent chemotactic factors for neutrophils (40, 44); KC and MIP-2 can effectively trigger neutrophil extravasation in a peritonitis model in vivo (1). In addition, transfection of the CXC chemokine CINC-1 gene into rat hepatocytes resulted in hepatic neutrophil recruitment and extravasation (41). Our previous data indicate that neutrophil extravasation is a prerequisite for neutrophil-mediated liver injury in the Gal/ET model (6). Inhibition of extravasation by blocking adhesion molecules attenuated liver injury by preventing neutrophil-mediated oxidant stress after Gal/ET (10, 11, 29) as well as in other liver disease models (15, 18). Thus, if CXC chemokines play a relevant role in the pathophysiology, it was expected that neutralizing KC and MIP-2 would result in less neutrophil extravasation and reduced neutrophil-induced injury without an effect on apoptosis. Indeed, the anti-KC and anti-MIP-2 antibodies did not affect apoptosis or the overall neutrophil recruitment into the liver. Because both effects are entirely TNF dependent in this model (30, 37, 48), these results are consistent with the hypothesis and previous observations that CXC chemokines may be of limited relevance for hepatic neutrophil recruitment if more potent activators of neutrophils are present (1). However, neutralizing antibodies did not prevent neutrophil extravasation and liver injury after Gal/ET. These data suggest that CXC chemokines are not the critical signal for migration of neutrophils into the parenchyma. Moreover, CXC chemokine formation was not significantly affected when apoptosis was almost completely prevented by the pancaspase inhibitor Z-VAD-fmk. Although these results appear to contradict those of a previous study where hepatocytes undergoing Fas receptor-mediated apoptosis generated CXC chemokines (13), the situation in the endotoxemia model is clearly different. Even the low doses of ET used in the Gal/ET model induce substantial formation of TNF-α and IL-1, both of which are potent inducers of KC and MIP-2. Under these circumstances, CXC chemokine formation due to apoptosis is most likely negligible compared with the direct cytokine effect. The results with neutralizing antibodies were completely confirmed in CXCR2−/− mice, which showed neutrophil localization and neutrophil-mediated injury similar to that in wild-type animals.
Although our experiments strongly suggest that the CXC chemokines MIP-2 and KC are not involved in the pathophysiology, we cannot exclude the possibility that other chemokines could play a role. Proinflammatory conditions can increase the expression of CC chemokine receptors 1 and 2 on neutrophils (5, 32). The neutrophils then respond to CC chemokines such as MIP-1α (32, 59), monocyte chemoattractant protein-1 (32), and leukotactin (59). Treatment with anti-MIP-1α antibodies resulted in reduced neutrophil infiltration and transmigration in models of Ig- (49) or ET-induced lung injury (51). The role of CC chemokines in the pathogenesis of Gal/ET-induced liver injury is unknown and needs to be investigated.
Interestingly, Li et al. (39) recently suggested that CXC chemokines may be the critical mediators of neutrophil extravasation in the Gal/ET model. However, there are serious concerns about the interpretation of the results. 1) The antichemokine antibodies used by Li et al. reduced parenchymal cell apoptosis (39). Because apoptosis in this model is entirely mediated by TNF-α (30, 37), these findings suggest that Li et al. may have reduced TNF levels with these antibodies. Although it remains unclear how this occurred, IgG has the capacity to bind ET and attenuate cytokine formation (42). Less TNF-α formation will result in reduced apoptosis, which is a critical event in neutrophil extravasation and injury (17, 30, 35). Thus at least some of the data of Li et al. can be explained without invoking any involvement of CXC chemokines in the pathophysiology of Gal/ET-induced liver injury. Another concern is that Li et al. found protection with each antibody alone. Given the fact that MIP-2 and KC are potent chemotactic factors for neutrophils and each can trigger neutrophil extravasation (1), one would expect a relevant effect on neutrophil extravasation only if both chemokines are eliminated. These concerns and other issues are discussed in more detail elsewhere (24).
In summary, our data indicate that cytokines produced during endotoxemia are responsible for the massive formation of KC and MIP-2 in the liver and possibly other extrahepatic sites. However, a pathophysiological role of these CXC chemokines could be excluded on the basis of five strong arguments: 1) The time course of CXC chemokine formation did not correlate with neutrophil extravasation. 2) ET and Gal/ET induced a similar CXC chemokine response, but only Gal/ET triggered apoptosis and neutrophil extravasation. 3) Neutralizing antibodies against KC and MIP-2 had no effect on neutrophil extravasation and injury. 4) Wild-type and CXCR2−/− mice showed similar neutrophil extravasation and liver injury. 5) Eliminating apoptosis with a pancaspase inhibitor prevented neutrophil transmigration without affecting CXC chemokine formation. Thus, on the basis of these different experimental approaches, which yielded identical results, we can conclude that CXC chemokines are not responsible for neutrophil recruitment into the liver or for neutrophil extravasation and, therefore, are not involved as a chemotactic signal in the injury process after Gal/ET administration.
The project was funded in part by National Institute on Alcohol Abuse and Alcoholism Grant AA-12916.
The authors thank Cathleen Cover for expert technical assistance.
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 © 2005 the American Physiological Society


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she seems angry about 60% of the time...
very nice
Holy shit she's hot. What an ass. 5/5.
Just be limber bebe.
LIke a lot of wives - even the porn gals have to fake it and shout "yes, yes." Baloney - hardly ever see a clit brought to orgasm - it is so easy for a guy to come, but it is not easy to get a gal to orgasm - takes a little time.
Wow, please post more if you have it! Insanely hot body!
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Awesome Blowjob Silent_Lamb go get laid, and shes hot overall 5/5
hey joe, idk where shes from, but she spoke spanish...so u kinda get an idea...
what a blowjob!!
lol at 19:30, starts moaning in some other language. any more of this girl somewhere?
wow shes fine.
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About 25 minutes into "Dracula 2: Ascension", Fair Hair Lead Elizabeth (Diane Neal) moans, "Why is this happening?" Well, Lizzie, let's recap what you've done in just the last 10 minutes alone, shall we? Let's see: discover a vampire in your morgue; steal the vampire; and then feed the vampire a bathtub full of blood. Gee, no wonder Elizabeth is so shocked that Dracula woke up, killed one of her friends, and tries to kill the rest. Stupid girl.
You have to really like genre movies to like "Ascension", but even then the movie will try your patience. A sequel to the theatrical film "Dracula 2000", "Ascension" is Straight-to-Video, and from what I can tell it has a slightly smaller budget and lower quality of writing. Other than that, the same filmmakers behind the original made the sequel. The filmmakers also made a third installment at the same time called "Dracula 3: Legacy", but at present there's no release date for the third.
Jason Scott Lee ("Dragon") stars as Uffizi, a priest and vampire hunter, who has tracked the burning corpse of Dracula (last seen roasting on a cross over Mardi Gras) to a morgue. Before Uffizi can destroy the undead bloodsucker's remains, enterprising coroner Luke (Jason London) and med student Elizabeth steals the body. Elizabeth's plan is to use Drac's powers to save Lowell (Craig Sheffer), the love of her life, but Luke just wants to get rich because a mysterious phone call has offered him $3 million for the body.
It's up to Uffizi to find the kids before they get offed by the resurrected Drac, although I have to say, with kids this dumb and intellectually — as well as morally — bankrupt, all I'm hoping for is that Dracula will kill them slow and long and make it very painful. Unfortunately writers Joel Soisson and Patrick Lussier don't quite share my enthusiasm for bloodletting. As a result the med students and Sheffer's character lives for way too long and their deaths, when we finally get them, aren't even worthwhile. Decapitated heads? That's all we get? You've got to be kidding me.
If you could stand the mundane scenes where the would-be-victims go through about 5 different personalities within the space of the movie's 85 minutes, then there is Jason Scott Lee's Uffizi to carry the day. As the vampire hunter/priest, Lee is the most interesting character in the film, not to mention its one and only saving grace. The most frustrating thing about "Ascension" is just how abysmal the other characters are when compared to Lee's, and director Lussier's inability to realize how bad the movie is when Lee isn't around to save it.
I wanted to know more about Uffizi, but all I got was a love triangle between the greedy Luke, the crippled Lowell, and the intellectually retarded Elizabeth. As the resurrected vampire, Stephen Billington doesn't do much except be tied to a post as he's experimented on. The screenwriters manage to explain the appearance of a new actor playing the Dracula character with a simple line of dialogue that mentions Dracula's change of appearance after every resurrection. Roy Scheider ("Jaws") also shows up briefly as Uffizi's mentor, but his scenes equal a total of 2 minutes, although that doesn't prevent the film from bragging about his appearance on its boxcover.
If it's not obvious by now "Ascension" is not a very good horror film. Its weakest elements are its characters, all of which (with the exception of Uffizi) wobbles from irritating to annoying to unbearably lame. Khary Payton plays the African-American Kenny, whose character manages to join the ranks of the Loudmouth Black Guy, that movie stereotype filled capably by Chris Tucker and Martin Lawrence.
It should also be noted that "Ascension" ends with a cliffhanger. How silly of the filmmakers, making us buy/rent 2 movies just to see one completed lousy film. Now that's gumption for ya.
Patrick Lussier (director) / Patrick Lussier, Joel Soisson (screenplay)
CAST: Stephen Billington …. Dracula
Jason Scott Lee …. Uffizi
Jason London …. Luke
Craig Sheffer …. Lowell
Diane Neal …. Elizabeth


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Legal Question in Real Estate Law in New York
Property Rights
I erected my fence 12 inches encroaching on my neighbors property for more then 12 years. Now I am rebuilding my house, my neighbor objects I should put the fence back in the previous position. Do I have a right by proscription?
2 Answers from Attorneys
Re: Property Rights
While some right of adverse possession may exist, the term to acquire these rights is usually more than the time you indicated. Your neighbor has the right to compel you to move the fence to your property or, if you refuse, to remove it himself. I suggest you move the fence to your property. This is a reply to an Internet question and the response is not intended to be legal advice or as creating an attorney-client relationship. Omitted or missing facts could result in a different reply.
Re: Property Rights
You have nothing unless you go to court to get it with a lawsuit..
Good Luck.
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Ordinary types of deeds What are the ordinary deed forms in New York? Asked 12/13/06, 9:44 pm in United States New York Real Estate and Real Property


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Remember when opening a new line of credit will always drop your score. Once you make the payments you will go back or above where you started. thus you're eligible for better opportunitys.
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You don't have to get a Costco credit card since Costco now accepts Visa cards, and that covers a LOT of cards.
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No. simply having a secured credit will not help you be approved for a Costco CC. Making payments on time will improve your credit score, improving your chances that way. But that takes time.
Whether or not you are approved for Costco CC, will based on your credit report at the time of applying.
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Increase over time... I know it won't help immediately.
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CL Increase
With requesting a credit limit increase, usually they just ask your yearly income.. assuming you already have the Costco card. Waiting 6 months between requests/when you opened the card is the minimuml.
The two factors you've described are mutually exclusive.
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Motor learning must be capable of increasing or decreasing the amplitude of movements to meet the demands of the environment. One way to implement such opposite learned changes would be to store them with bidirectional plasticity mechanisms (i.e., long-term potentiation and depression at the same synapses). At the behavioral level, this scheme should result in similar patterns of stimulus generalization of increases and decreases in movement amplitude because the same synapses would be modified but in opposite directions. To test this idea, we quantitatively compared the stimulus generalization of learned increases and decreases in the gain (amplitude) of the vestibuloocular reflex (VOR) in mice and in monkeys. When examined across different sinusoidal frequencies of head rotation, decreases in VOR gain generalized more than increases in gain. This difference was apparent not only in the gain, but also the phase (timing) of the VOR. Furthermore, this difference held when animals were trained with high-frequency rotational stimuli, a manipulation that enhances frequency generalization. Our results suggest that increases and decreases in VOR gain are not exact inverses at the circuit level. At one or more sites, the plasticity mechanisms supporting decreases in VOR gain must be less synapse-specific, or affect neurons more broadly tuned for head rotation frequency, than the mechanisms supporting increases in gain.
Cerebellum-dependent motor learning is essential for improving and maintaining the accuracy of movement throughout life. Over time, both adaptive increases and decreases in movement amplitude may be required as the organism, its environment, or both, change. A longstanding model of motor learning assumes that both increases and decreases in movement amplitude are implemented by a single plasticity mechanism, applied to synapses carrying different sensory or motor signals (Albus 1971; Ito 1982; Marr 1969). However, a recent behavioral analysis of the reversal of motor learning suggests a new hypothesis: opposite learned changes in movement amplitude may engage long-term potentiation (LTP) and long-term depression (LTD) at the very same synapses (Boyden and Raymond 2003). Bidirectional plasticity has been discovered at sites throughout the cerebellar circuit (Aizenman et al. 1998; Caria et al. 2001; Coesmans et al. 2004; Jorntell and Ekerot 2002; Lev-Ram et al. 2002, 2003; Rancillac and Crepel 2004), and there is evidence that plasticity mechanisms at more than one site contribute to cerebellum-dependent motor learning (reviewed in Boyden et al. 2004). This raises an important question: do increases and decreases in movement amplitude alter the same set of synapses, but in opposite directions, at all sites of plasticity in the circuit—i.e., are they exact inverses at the circuit level?
One way to assess whether learned increases and decreases in movement amplitude are exact inverses is to examine their patterns of generalization to contexts different from those used to induce learning. If, at all sites of plasticity in the circuit, the same synapses are altered for increases and decreases in movement amplitude but in opposite directions, then the behavioral changes in both directions should have similar patterns of generalization. On the other hand, if different sets of synapses are modified during increases and decreases in movement amplitude, then these synapses may be tuned differently for the contexts in which the behavior is produced, and therefore the learned behavioral changes may exhibit different patterns of generalization.
Here, we analyze a simple eye movement, the vestibuloocular reflex (VOR), the amplitude (gain) of which can be adaptively increased or decreased by cerebellum-dependent learning. In particular, we examine the patterns of stimulus generalization to evaluate whether opposite learned changes in the amplitude of this movement are exact inverses of each other at the circuit level. The VOR stabilizes images on the retina during head movement by producing eye movement in the direction opposite to the head. If the VOR is poorly calibrated, head movements cause image motion on the retina. In such conditions, motor learning can adaptively adjust the gain of the VOR to improve image stability. In the laboratory, one can induce motor learning in the VOR by exposing animals to paired visual and vestibular stimuli. The acquisition of both adaptive increases and decreases in VOR gain depends on the cerebellum as evidenced by lesion and inactivation studies in many species (Ito et al. 1974; Koekkoek et al. 1997; McElligott et al. 1998; Michnovicz and Bennett 1987; Rambold et al. 2002; Robinson 1976). Despite this common requirement for the cerebellum, there are behavioral differences between increases and decreases in VOR gain consistent with the reliance of these two closely related motor learning tasks on different plasticity mechanisms (Boyden and Raymond 2003; Cohen et al. 2004; Eggers et al. 2003; Kuki et al. 2004; Miles and Eighmy 1980). Furthermore, a few studies have provided evidence for their reliance on different molecular mechanisms (Boyden et al. 2003; Carter and McElligott 1995; Li et al. 1995). Thus increases and decreases in VOR gain appear to rely on different neural mechanisms. However, it is not known whether these different mechanisms are inverses of one another at all sites of plasticity in the circuit.
In this study, we compared the stimulus generalization of increases and decreases in VOR gain across head-rotation frequency. Previous studies have demonstrated that learning is best expressed at the sinusoidal frequency of head rotation used for training, and less so at different test frequencies (De Zeeuw et al. 1998; Feil et al. 2003; Iwashita et al. 2001; Lisberger et al. 1983; Raymond and Lisberger 1996; Wallman et al. 1982). However, the generalization of increases in VOR gain across stimulus frequency had not been explicitly compared with the generalization of decreases in VOR gain. We quantitatively compared the two and found that decreases in VOR gain generalized across head-rotation frequency more than increases in gain. This suggests that increases and decreases in gain are not exact inverses at the circuit level.
Mouse experimental setup
All animal protocols were approved by the Stanford University Administrative Panel for Laboratory Animal Care. Experiments were performed on 33 adult (≥8 wk old) B6129PF2/J male mice with black eyes (Jackson Lab, Bar Harbor, ME).
B6129PF2/J mice are F2 hybrids of C57BL/6 and 129 inbred strains. For these mice, the pretraining VOR gain (defined as the ratio of peak eye velocity to peak head velocity and measured as described in Data analysis) was 0.18 ± 0.02 at 0.5 Hz (mean ± SD; ±10°/s peak head velocity), and 0.27 ± 0.02 at 2 Hz. These values were similar to those reported in previous studies using B6 strain mice and measuring the VOR gain with eye coils (De Zeeuw et al. 1998; Koekkoek et al. 1997). These values were slightly lower than those reported for C57 mice, measured using eye coils (Boyden and Raymond 2003; Coesmans et al. 2003; Harrod and Baker 2003; van Alphen et al. 2001). Studies of the VOR using video methods have reported higher VOR gains (Katoh et al. 1998; Stahl et al. 2000), and one study of eye movements in the light has suggested that an eye coil or the associated surgical implantation technique can load the eye or otherwise reduce eye-movement gains (Stahl et al. 2000). On the other hand, the accuracy of the video method is limited by several factors including changes in the size of the pupil, which can vary during and between experiments and affect the measurement of eye position. Furthermore, video methods preclude the measurement of VOR gain immediately before a visual-vestibular training session because it requires pupil-constricting drugs to measure the VOR in the dark, and these drugs compromise vision in lighted conditions appropriate for training. Eye-coil methods were therefore preferred because the goal in this study was the measurement of learning-related changes in the VOR by comparison of the VOR in the dark immediately before and after visual-vestibular training.
Surgical methods were identical to those described previously (Boyden and Raymond 2003). Briefly, while the mouse was under anesthesia, a head post was attached to the top of the skull using anchor screws and dental acrylic, and a scleral search coil (IET, Marly, Switzerland) weighing ∼50 mg was implanted on the temporal side of the right eye just underneath the conjunctiva. The search coil leads were run subcutaneously to a two-pin connector. Mice were allowed to recover from surgery for 5–7 days. Mice with eye scarring after surgery were excluded from the study (5/38 mice).
For experiments, the head of the mouse was immobilized by attaching the implanted head post to a restrainer. The restrainer was attached to a turntable (Carco IGTS, Pittsburgh, PA), which delivered a vestibular stimulus by rotating the mouse about an earth vertical axis. The restrained mouse was positioned in the center of a magnetic field generated by a set of 18-in magnetic coils (CNC Engineering, Seattle, WA), which was fixed to the turntable. The magnetic coils generated signals in the scleral search coil that were related to the eye position. An analog differentiator and filter with a 300-Hz corner frequency were used to obtain eye velocity from eye position. All signals were digitized at a sampling frequency of 500 Hz. The raw velocity traces used only for illustration purposes in Fig. 1 were obtained by averaging both eye and head velocity within a sliding window of 50 ms. Visual motion was delivered by a moving optokinetic drum made of a white translucent plastic half-dome with black vertical stripes, each of which subtended 7.5° of visual angle. The optokinetic drum was back-lit by two 60-W lamps. A silvered acrylic plate attached to the turntable helped to ensure that the motion of the drum filled most of the mouse's field of view (∼600° of solid angle).
Mouse behavioral testing
After recovery from surgery and prior to any behavioral experiments, each mouse was acclimatized to the experimental set-up for 15–40 min. During this period, the eye coil was calibrated by rotating the magnetic coils around the stationary mouse in a sinusoidal manner at 0.5 and 2 Hz, ±10°/s peak velocity.
One to 2 days after acclimatization, we began experiments on motor learning in the VOR. Before and after training, we measured the VOR in the dark in response to vestibular stimuli with sinusoidal velocity profiles at 0.5-, 1-, 2-, and 5-Hz test frequencies with ±10°/s peak velocity (Fig. 1A). At least 8 s before taking a data file, a bright light was flashed to keep the animal alert. Gain increases were induced by presenting sinusoidal visual and vestibular stimuli that were at the same speed and 180° out of phase (gain-up training; Fig. 1B). Gain decreases were induced by presenting sinusoidal visual and vestibular stimuli that were at the same speed and exactly in phase (gain-down training). The training frequency was either 0.5 or 2 Hz with peak velocity of ±10°/s. The training stimuli were presented in two 15-min blocks, and the VOR in the dark at the training frequency was measured between blocks (90–105 s).
Between experiments, the VOR gain was allowed to return to baseline by permitting mice to experience a normal visual-vestibular environment for at least 2 days after gain-up training or 3 days after gain-down training before the next experiment. A longer recovery period was used after gain-down training because previous reports have shown that decreases in VOR gain decay more slowly than increases in gain (Boyden and Raymond 2003; Miles and Eighmy 1980), especially with extended gain-down training. However, with a single 30-min training session, as used in the present experiments, recovery is fairly rapid. Within 2 days after gain-up training, the VOR gain was not different from the original gain (P > 0.23, paired t-test), and within 3 days after gain-down training, the VOR gain was not different from the original gain (P > 0.71). In general, gain-up and gain-down training sessions were alternated. To determine whether learning in naïve mice is the same as that in previously trained mice, we compared the percent change in VOR gain of both groups of mice, and found no difference (P > 0.05, unpaired t-tests). The recovery period of 2–3 days after 30 min of training is therefore sufficient to restore not only the VOR gain but also the capacity of the VOR circuit for learning.
Mouse data analysis
Custom software was used to analyze eye- and head-velocity traces. Eye-velocity traces were visually inspected for any deviations, such as saccades and movement artifacts. Such deviations were marked, and the whole sinusoidal cycle containing the deviation was excluded from the analysis. Eye- and head-velocity cycles were averaged and subjected to Fourier analysis. Harmonic distortion (defined as the ratio of the amplitude of the 2nd harmonic to the amplitude of the 1st harmonic) was fairly small and did not change with learning (pretraining: 15% at 0.5 Hz, 6% at 2 Hz, n = 6 representative mice; after gain-up: 11% at 0.5 Hz, 6% at 2 Hz; after gain-down: 18% at 0.5 Hz, 5% at 2 Hz). Therefore the amplitude and timing of the fundamental frequency component was used to calculate the averaged VOR gains and phases. The VOR gain was defined as the ratio of eye- over head-velocity amplitudes. The VOR phase was defined as the difference between eye-velocity phase and head-velocity phase, with phase equal to zero when the peak eye velocity occurred at the same time as the peak head velocity in the opposite direction. Positive VOR phase values indicate a phase lead of eye relative to head velocity and negative values, a phase lag. Plots illustrating learned changes in mouse VOR gain and phase show data that are normalized to the pretraining value. All raw gains and phases, before and after training, are provided in Tables 1 and 3. We analyzed the amplitude and timing separately to determine how learning affected each of these aspects of eye movement.
The following criteria were applied to determine which experiments would be considered for further analysis. Experiments where less than a total of 10 cycles per test frequency remained for calculating the VOR gain before and after learning were excluded (9/106 experiments). Experiments where we were unable to obtain a reliable measurement of the VOR gain before training were also excluded. More specifically: if the variance of the VOR gain from 5 to 10 18-s data files taken prior to training was more than half of the average VOR gain across these files, then the measurement was deemed unreliable (4/106 experiments from 4 mice). Because generalization of learning to a test condition is only meaningful if a change is observed in the training condition, we excluded data from experiments in which the mouse did not exhibit changes in VOR gain in the adaptive direction at the training frequency (18/106 experiments; 17 gain-up, 1 gain-down). The criterion for rejection was the final gain at the end of the half hour had changed in the maladaptive direction relative to baseline. Data that met all of our criteria (75/106 experiments) were weighted equally across mice by averaging the changes in gains and phases for replications in each mouse before averaging across mice. For 2-Hz experiments, one replication of each training condition was included in the analysis: n = 18 mice for gain-up, n = 16 mice for gain-down. One mouse did not have posttraining 1-Hz data after gain-down training at 2 Hz and was excluded from the analysis of the generalization index (see following text). For 0.5-Hz experiments, one to two replications of a given training condition per mouse were included in the data analysis: for gain-up, one replication from n = 7/14 mice, two from n = 7/14 mice, and for gain-down, one replication from n = 18/19 mice, two from n = 1/19 mice.
To compare the overall pattern of generalization of increases and decreases in VOR gain, we defined a generalization index as the fraction of learning at the training frequency that is expressed, on average, at test frequencies other than the training frequency, calculated as Δgaini represents the percent change in VOR gain measured at one of the j head rotation frequencies other than the training frequency (e.g., for 2-Hz training, i = 0.5, 1, and 5 Hz, j = 3) and Δgaintrain, the percent change in gain at the training frequency of 0.5 or 2 Hz. Increasing values of the generalization index indicate increasing extents of generalization. When the average change in gain at nontraining frequencies is equal to Δgaintrain, the index is 1, indicating broad generalization. When the average change in gain at the test frequencies other than the training frequency is 0, the index is 0, indicating specificity. When the average change in gain at nontraining frequencies is larger than the change at the training frequency, the index is >1, and when the average change in gain at nontraining frequencies is maladaptive, the index is <0.
Statistical analysis was performed using StatView (SAS Inst., Cary, NC). To determine whether changes in the VOR gain and phase were significantly different from zero, we performed a one-sample t-test with Bonferroni correction for multiple comparisons. A one-factor ANOVA was performed to determine whether VOR gain changes varied significantly with frequency of head rotation. In cases where changes in gain did vary significantly with frequency, we determined whether the changes at the test frequencies were significantly different from the change at the training frequency using Dunnett's post hoc test. Dunnett's test allows comparisons of the mean from each group to the mean of a "control" group (Dunnett 1955). To determine the overall magnitude of the effect of learning on phase changes at nontraining frequencies, the weighted average of the absolute phase change across all nontraining frequencies was calculated for each training condition and compared. A Mann-Whitney test was used for comparing absolute phase and generalization index values between training conditions.
Primate protocols
Rhesus macaque surgical preparation, calibration, behavioral experimentation, and data analysis were performed as described in Raymond and Lisberger (1996) except that learning was induced with 2 h of visual-vestibular training, and changes in VOR gain were assayed at five frequencies (0.2, 0.5, 1, 2, and 5 Hz). All frequencies tested were used in the calculation of the generalization index. In the current study, monkeys underwent gain-up and gain-down training at 0.5 Hz (n = 2 monkeys) and 5 Hz (n = 1). For the data extracted from Raymond and Lisberger (1996), monkeys underwent gain-up and gain-down training at 0.5 Hz (n = 3 monkeys), 2 Hz (n = 2), 5 Hz (n = 3), 8 Hz (n = 2), and 10 Hz (n = 2). Data from one monkey for the 10-Hz training frequency were excluded from the analysis of generalization index because there was no change in gain at the 10-Hz training frequency, yielding an invalid generalization index value (i.e., dividing by 0). We analyzed the data with Mann-Whitney tests.
Learned decreases in VOR gain generalize more than increases in VOR gain
Motor learning in the VOR was induced in mice by pairing horizontal head rotations with a moving visual stimulus to either increase (gain-up training) or decrease (gain-down training) the gain (amplitude) of the VOR (Fig. 1). In all experiments, the movements of the head and visual stimulus had sinusoidal velocity profiles, and the frequency of head and visual stimulus rotation used to induce learning (training frequency) was either 0.5 or 2 Hz. Before and after training, the gain of the VOR was measured in the dark across a range of test frequencies: 0.5, 1, 2, and 5 Hz (Table 1).
The central finding was that increases in the gain of the VOR were expressed primarily at the training frequency, whereas decreases in gain were expressed more broadly across test frequency. After gain-up training at 0.5 Hz, a significant increase in gain was observed only at 0.5 Hz, indicating that the learned change was specific to the training frequency (Figs. 1B and 2A; n = 14 mice, P < 0.01, one-sample t-test with Bonferroni correction for multiple comparisons). After gain-down training at 0.5 Hz, significant decreases in the gain of the VOR were evident across all frequencies tested (n = 19 mice, P < 0.01). The decrease at the 0.5-Hz training frequency was not significantly different from the decrease at the 1-Hz test frequency F(3,72) = 4.45, P < 0.01, one-factor ANOVA; P > 0.05, post hoc Dunnett's test. The generalization, however, was not complete because the gain decrease at 0.5 Hz was significantly larger than the gain decrease at the 2- and 5-Hz test frequencies. Yet even though the generalization of gain decreases was incomplete, these learned decreases generalized more than the increases in VOR gain induced with the same 0.5-Hz stimulus frequency.
Previous work has suggested that different plasticity mechanisms are engaged by high- and low-frequency training (Boyden et al. 2003; Raymond and Lisberger 1996, 1998). In addition, it has been shown that training at higher stimulus frequencies leads to more generalization of VOR motor learning (Raymond and Lisberger 1996). Therefore, we determined whether the greater generalization of gain decreases relative to gain increases was still observed for learning induced with a higher training frequency. We trained mice at a higher head-rotation frequency of 2 Hz and found that learned decreases in the gain of the VOR still generalized more than increases in gain (Fig. 2B). After gain-up training, a significant gain increase was observed only at the training frequency of 2 Hz (n = 18 mice, P < 0.01, one-sample t-test with Bonferroni correction for multiple comparisons). In contrast, after gain-down training at a frequency of 2 Hz, significant learned decreases in gain were expressed across all frequencies tested (n = 16, except n = 15 for 1 Hz, P < 0.01). In addition, the percent decreases at each frequency were not significantly different from each other F(3,59) = 2.58, P > 0.05, one-factor ANOVA). Thus even at the higher training frequency of 2 Hz, more generalization was observed for decreases in VOR gain, suggesting that the difference in generalization between increases and decreases in gain is common to the potentially different sets of plasticity mechanisms mediating the effects of training at high and low frequencies.
To quantify the overall pattern of generalization, we calculated a generalization index that reflects the fraction of learning at the training frequency that is expressed, on average, at test frequencies other than the training frequency (described in methods). Higher index values represent more generalization. When the changes in gain across all frequencies are equal, the index is 1. When the changes in gain at test frequencies other than the training frequency are zero, the index is 0. For both lower (0.5 Hz) and higher (2 Hz) training frequencies, decreases in VOR gain were associated with significantly higher generalization index values than increases in gain (Fig. 3, A and B; P < 0.05, Mann-Whitney test). Thus when the overall pattern of generalization was quantified, the generalization of gain decreases was more extensive than that of gain increases regardless of the training frequency.
To confirm whether learning induced with a higher stimulus frequency does indeed generalize more than learning induced with a lower stimulus frequency, as previous work in monkeys suggested (Raymond and Lisberger 1996), we compared generalization indice x values of mice trained with a lower (0.5 Hz) and a higher (2 Hz) stimulus frequency for each direction of learning (Fig. 3, A and B). The learned increases in VOR gain induced with a 2-Hz stimulus were associated with significantly higher generalization index values than the increases induced with a 0.5-Hz stimulus (P < 0.05, Mann-Whitney test). In contrast, learned decreases in VOR gain induced with 0.5- and 2-Hz training stimuli resulted in comparable high levels of generalization, perhaps reflecting a ceiling effect.
In rhesus monkey, previous papers have examined the generalization of motor learning in the VOR across stimulus frequency (Lisberger et al. 1983; Raymond and Lisberger 1996). However, no direct statistical comparison of the generalization of increases and decreases in gain was performed. We calculated generalization indice x values for data published in our earlier study on rhesus macaques (originally plotted in Raymond and Lisberger 1996; Fig. 7) to determine whether our generalization index could resolve differences between increases and decreases in gain in those earlier data. We also ran generalization experiments on two additional monkeys. For four of five training frequencies tested, the generalization index for a learned decrease in VOR gain was higher than for an increase in gain (Table 2). These differences were not significant at any individual training frequency (P > 0.12, Mann-Whitney test). However, when experiments with the five different training frequencies were pooled, monkeys exhibited a significantly higher generalization index for decreases in gain than for increases in gain (Fig. 3C; P < 0.05). Therefore the greater generalization of learned decreases than increases in VOR gain is present across species.
The different amounts of generalization of increases and decreases in gain could not be explained by different amounts of learning in the two directions. In mice, with training at 2 Hz, decreases in gain generalized more than increases in gain even though the percent changes in gain at the training frequency were similar for the two directions (Fig. 2B, Table 1). When the training frequency was 0.5 Hz, however, the percent decrease in the VOR gain at 0.5 Hz was larger than the percent increase in VOR gain. Nevertheless, we did not find any significant correlation between the amount of learning and the amount of generalization in individual mice (R = 0.39 for gain-up, R = −0.12 for gain-down, P > 0.18). Furthermore, when the analysis was restricted to only those experiments with learned increases and decreases in gain of similar amplitudes at the training frequency, the result was the same. Experiments with a training frequency of 0.5 Hz were ranked by percent change in gain at the training frequency, and experiments with the largest decreases in gain and the smallest increases in gain were discarded until the mean amplitude of the percent change in gain at the training frequency was similar for both training paradigms (mean ± SE for gain-up: 34 ± 9%, n = 9; gain-down: −34 ± 2%, n = 13; P > 0.05 Mann-Whitney test; Fig. 2A, inset). Even when the percent changes in gain in the two directions were thus matched, gain decreases were still associated with a significantly higher generalization index (0.53 ± 0.13) than gain increases (-0.30 ± 0.27; P < 0.01, Mann-Whitney test). Thus the greater generalization of decreases in VOR gain is not the result of more learning.
Gain decreases influence VOR phase more than gain increases
Consistent with our observations regarding changes in VOR gain, changes in the timing of the VOR (as reflected by the phase) were more pronounced across test frequency after gain-down training than after gain-up training. Before and after training, the phase of the VOR was measured at each test frequency (Table 3). When motor learning was induced with a 0.5-Hz training stimulus, there were no significant changes in VOR phase at 0.5 Hz or any of the other test frequencies after gain-up training (Fig. 4 A; P > 0.0125 one sample t-test with Bonferroni correction for multiple comparisons). After gain-down training, however, significant increases in phase lead were found at test frequencies of 0.5, 1, and 2 Hz. Thus gain-down training produces larger phase changes across frequency of head rotation than gain-up training.
Both gain-up and gain-down training at 2 Hz induced substantial changes in phase only at head rotation frequencies other than the training frequency. Learned changes in phase were in opposite directions for test frequencies above versus below the training frequency (Fig. 4B; P < 0.01). This "phase-change cross-over" has been noted in previous reports (Iwashita et al. 2001; Lisberger et al. 1983; Raymond and Lisberger 1996). In addition, we found that gain-down training affected the changes in phase at the nontraining frequencies more than gain-up training. After gain-down training, more test frequencies exhibited significant changes in phase than after gain-up training. Furthermore, the mean amplitude of the change in phase after gain-down training (mean absolute value = 9.4 ± 0.92°) across all test frequencies other than the training frequency was significantly larger compared with the mean after gain increases (6.8 ± 0.67°; P < 0.05, Mann-Whitney test). Thus for both 0.5- and 2-Hz training frequencies, the greater generalization of gain-down training across head rotation frequency is manifested not only in terms of more widely expressed changes in gain but also in terms of more widely expressed changes in phase.
We quantitatively compared the generalization of learned increases and decreases in VOR gain and found that gain decreases generalized more across head-rotation frequency than gain increases. Our data support the idea that opposite learned changes in the VOR are not exact inverses at the circuit level. If increases and decreases in VOR gain altered the same set of synapses in opposite directions, then changes in gain in both directions should generalize across frequency to a similar extent contrary to what we found. Our data thus refine the idea that opposite learned behavioral changes could be stored using bidirectional plasticity mechanisms in the cerebellum, such as LTP and LTD (Aizenman et al. 1998; Boyden and Raymond 2003; Caria et al. 2001; Coesmans et al. 2004; Jorntell and Ekerot 2002; Lev-Ram et al. 2002, 2003; Rancillac and Crepel 2004). Increases and decreases in VOR gain may be stored using bidirectional plasticity mechanisms at some sites of plasticity—indeed, modeling and behavioral studies of the cerebellum suggest that opposite behavioral changes are at least partial inverses at the circuit level (Boyden and Raymond 2003; Mauk and Ohyama 2004). However, they must violate this relationship at one or more sites of plasticity in the circuit.
Our study is the first to provide a direct, statistical comparison of the generalization of increases and decreases in the gain of the VOR, although previously published data provided some suggestion of a difference (Iwashita et al. 2001; Lisberger et al. 1983; Raymond and Lisberger 1996). The re-analysis of our earlier rhesus monkey data, combined with new rhesus experiments, revealed significantly greater generalization of decreases than increases in VOR gain, and, in mice, these differences could be resolved for individual training frequencies. The difference between increases and decreases in gain was observed whether training was done with low- or high-frequency stimuli. Thus, although different combinations of plasticity mechanisms may mediate the effects of training at low and high frequencies (Boyden et al. 2003; Raymond and Lisberger 1996, 1998), the mechanisms that underlie the greater generalization of gain decreases are common to both. Furthermore, this difference in generalization was apparent in the changes in VOR phase after gain-up and gain-down training. Gain-down, but not gain-up, training at 0.5 Hz resulted in a significant phase change across all test frequencies, and gain-down training at 2 Hz resulted in significantly larger changes in phase at nontraining frequencies than gain-up training. At the higher training frequency of 2 Hz, we observed a phase change cross-over, which had been previously hypothesized to result from the existence of multiple, independently modifiable frequency channels in the VOR circuit (Lisberger et al. 1983). In this scheme, phase changes at a given test frequency would result from the modification of frequency channels tuned for the training frequency but with broad enough tuning to also contribute to VOR performance at the test frequency. Our results suggest an extension of this model, namely that there would need to be broader tuning in the frequency channels modified by gain-down training than in the channels modified by gain-up training.
Neurons in the circuit for the VOR have been found to have different tuning properties, supporting the possibility that gain-up and gain-down training could affect differently tuned neurons. Synaptic plasticity in neurons tightly tuned for head rotation frequency may contribute selectively to gain increases, whereas changes in broadly tuned neurons may contribute selectively to gain decreases. In the vestibular nucleus, neurons exhibit a range of tuning to head-rotation frequency: some neurons show frequency selectivity, but others respond to a wide range of frequencies (Broussard et al. 2004; Dickman and Angelaki 2004). In the cerebellar cortex, the large number of cerebellar granule cells may permit each neuron to be tightly tuned for a particular context in which a movement is made (Albus 1971; Marr 1969). Therefore, one influential hypothesis has been that learning expressed in response to a narrow range of stimuli would be mediated by plasticity in the cerebellar cortex, whereas learning that generalizes broadly would be mediated by plasticity at a downstream site such as the deep cerebellar nuclei/vestibular nuclei (DCN/VN) (Thach et al. 1992). Interpreted in this framework, our current data would suggest that increases in VOR gain are more dependent on plasticity in the cerebellar cortex, whereas decreases in VOR gain are more dependent on plasticity in the vestibular nucleus. However, this "cortex-nucleus" model is at odds with several studies of cerebellum-dependent learning. Posttraining lesions of the cerebellum resulted in similar effects on both learned increases and decreases in VOR gain even across studies that found different degrees of impairment (Luebke and Robinson 1994; McElligott et al. 1998; Michnovicz and Bennett 1987; Partsalis et al. 1995; Pastor et al. 1994). Furthermore, in another form cerebellum-dependent learning, eye-blink conditioning, disconnecting the cerebellar cortical input to the DCN did not degrade the specificity of learned eye blinks for the tone used in conditioning, suggesting that plasticity in the DCN/VN can support stimulus-specific learning (Ohyama et al. 2003). Thus it is unlikely that increases and decreases in VOR gain rely on entirely separate sites in the VOR circuit.
Another way in which gain-up and gain-down training may affect different sets of synapses is that gain-down training could engage plasticity mechanisms that affect signaling through synapses not activated during training, whereas gain-up training could engage plasticity mechanisms that affect only synapses activated during training. In the cerebellum, there is evidence for both synaptic and nonsynaptic plasticity that affects information processing at synapses that were not activated during the plasticity-inducing event. These include both passive spread of plasticity from activated synapses to nearby nonactivated synapses (Jacoby et al. 2001; Reynolds and Hartell 2000; Wang et al. 2000) and changes in intrinsic excitability, which would affect the neuronal spiking response to any synaptic input (Aizenman and Linden 2000; Nelson et al. 2003; Smith and Otis 2003). Our results suggest that the plasticity mechanisms contributing to decreases in VOR gain may be less synapse-specific than those contributing to increases in gain.
The idea that changes at different synapses may contribute to oppositely directed motor learning in the VOR is consistent with a number of previous findings. Across multiple stimulus dimensions, there is a consistent pattern of greater generalization of learning for decreases versus increases in VOR gain. Studies have shown that gain decreases generalize more than gain increases when tested at head tilts different from those used during training (Yakushin et al. 2000, 2003). In addition, gain decreases induced by visual stimuli delivered to a single eye are expressed in the movements of the untrained eye, whereas gain increases do not generalize to the other eye (McElligott and Wilson 2001). Furthermore, the concept that opposite learned changes in behavior are stored with distributed changes that are not exact inverses at the circuit level is consistent with studies of other cerebellum-dependent learning tasks, such as extinction and savings of eye-blink conditioning (Mauk and Ohyama 2004; Perrett et al. 1993), and saccadic adaptation, in which learned increases and decreases in movement amplitude possess different behavioral properties (for review, see Hopp and Fuchs 2004). Further studies of these differences between opposite learned behavioral changes should yield insights into the neural mechanisms that iteratively refine learned movements over time.
This work was supported by National Science Foundation Grant DBI-0208400 to R. R. Kimpo; a Fannie and John Hertz Fellowship, National Institutes of Health Grant F31DC-7006, and the Dan David Prize Scholarship to E. S. Boyden; an International Human Frontier Science Program Organization Long-Term Fellowship and Zaffaroni Innovation Fund to A. Katoh; Howard Hughes Medical Institute Fellowship for Medical Students and the Stanford Medical Scientist Training Program Grant to M. C. Ke; and National Institutes of Health Grant R01DC-004154 to J. L. Raymond.
Helpful discussions on the manuscript were provided by A. S. Bristol and D. Winkowski. Excellent technical assistance was provided by R. S. Booth, P. W. Louderback, and K. Oh.
↵* These authors contributed equally to this work.
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 © 2005 by the American Physiological Society


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Welcome to The Villa Properties
The Villa is an enchanting residential retreat, inspired by generous spaces for outdoor living, the coolness and tranquillity of Spanish style courtyard housing and an environment alive with the sound of water from fountains in squares and from waterfalls cascading over rocky outcrops. The residential community surrounded by a mystical desert landscape, ideal for those looking for tranquillity close to the city. With walkways into the landscape, winding their way around the attractive desert landscape, restaurants, shops and pools all within walking distance of your home at The Villa, you can combine a relaxed and serene lifestyle with the Spanish countryside experience.
The Villa is located between three major roads of Dubai, Emirates Road, Outer Ring Road or the By-Pass road & Dubai – Al Ain road. This is the only project which is connected to three major roads of Dubai making access in the city as well as to other cities and towns of U.A.E easily approachable, without even entering into the traffic mess of the city. The Villa after Emirates Hills is the only project which sells plots and one can build a Villa of his own requirements by following the town planning of that area. Very closely located from the heart of the city, one can reach Karama or Health Care City within a span of 15 – 20 minutes from "The Villa".


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Hyderabad: Dept. of Urdu, University of Hyderabad organized a meeting to condole the death of Prof. Syeda Jaffar. The meeting was held on 27th June under the chairmanship of Prof. Muzaffar Ali, Head of the Dept. of Urdu.
In the meeting, a mention was made about her literary, research and critical contribution to Urdu language and literature. Prof. Muzaffar Ali in his condolence resolution mentioned that she served at Nizam College, Osmania University and University of Hyderabad. She was the Head of the Dept. of Urdu of Osmania University and University of Hyderabad. She spent all her life in teaching and writing. She authored 30 books. She was also associated with National Council of Promotion of Urdu Language, Sahitya Academy, South India Urdu Academy etc. She was awarded "Writer in Residence" fellowship by Sahitya Academy.
Dr. Habeeb Nisar, Professor of Urdu of HCU paid rich tributes to Prof. Syeda Jaffar and said that she was the greatest researcher of Deccani Urdu. With her demise, an era of Deccani studies came to an end.
Dr. Arshiya told that she was aggrieved with the demise Prof. Syeda Jaffar. Dr. Mohammed Kashif prayed for her. Present on this occasion were Dr. Mohammed Zahidul Haq, Asst. Professor of Urdu, a large number of research scholars and students.
–Siasat News


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Jetting 8" PVC w/ a 3000 psi 4.0 gpm washer? Homeowner questions...
Discussion in 'Drain Cleaning' started by robzr, Jul 14, 2013.
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Horticultural and botanical musings from the Rockies, Great Plains and beyond. In humble tribute to Goddess Flora.
Showing posts from August, 2013
Revisiting Kazakhstan--three years later...(photogallery)
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Optional items are: B. Bianca Euro Sham(s) SKU 001726, C. Bianca Framed Pillow SKU 001728, D. Bianca Pleated Pillow SKU 001727, E. Bianca Medalion Pillow SKU 001731, G. Bianca Buttoned Pillow SKU 001732. *Super sized, more duvet, these are larger than normal sized duvets, for a better fit for standard or pillow top mattresses. Fabric: 100% Polyester. Dry Clean Only.
Finish this fashion bedding set off with optional Bianca Euro Sham(s), and Bianca Pleated or Bianca Framed Pillow. Optional Sheet Sets are also available. Finish the room decor with Coordinating Curtains.


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Iver Wevley
Funeral services for Iver Wevley of Morris will be held Saturday, November 11, 2006 at 10:00 a.m. at Faith Lutheran Church in Morris. Reverend Ronald Boettner will be officiating. Visitation will be for one hour prior to services at the church on Saturday. Burial will be at Summit Cemetery in Morris.
Iver Kornelius Wevley, son of Carl and Carolina (Amundson) Wevley, was born August 12, 1915 in Highlandville, Iowa, where he was baptized on September 12, 1915 at Big Canoe Church. At a young age, his family moved to Barnsville, Minn., where he attended country school and was also confirmed on September 13, 1930 at Our Savior's Lutheran Church. On November 2, 1937, he was united in marriage to Adeline Pauling at the Lutheran Church in Barnesville. The couple remained in Barnesville, where they farmed and began raising their family. They later moved to the Morris area, where Iver worked at the West Central Experimental Station for 27 years. He retired in 1977.
Iver was a member of Faith Lutheran Church in Morris. He enjoyed fishing, keeping his lawn in shape, having fun and singing to his grandchildren. He especially enjoyed the time he spent with family and friends.
Iver died on Thursday, November 09, 2006 at West Wind Village in Morris, having lived to reach the age of 91 years.
He is survived by his wife: Adeline Wevley of Morris; five children: James (Pam) Wevley of St. Pete, Fla., Betty Gulbrandson of Watertown, Carol (Larry) Anderson of Wendell, Donna Knabe of Morris and Steve (Sara) Wevley of Hoffman; daughter-in-law: Ina Dunham of Minneapolis; 27 grandchildren; 37 great-grandchildren; five great-great-grandchildren; seven brothers and sisters: Melvina Larson of Morris, Delbert Wevley of Kingman, Kan., Darlene Wold of Springfield, Ore., Ione Quam of Ashby, Knute Wevley of Apple Valley, Mary Pashe of Ashland, Ore. and Earl Wevley of Menahga and several nieces and nephews. He was preceded in death by one son: Eugene Wevley; son-in-law: Ken Gulbrandson; grandson: Todd Gulbrandson; his parents; three sisters: Violet Miller, Gladys Hatestad and Gertrude Wevley; three brothers: Oren, Ray and Carl Wevley and one brother-in-law: Clarence Quam.
Pallbearers for the service are: Scott Bergherr, Vernon Wevley, Kevin Wevley, Tom Gulbrandson, Christopher Hacker and Dylan Wevley. Honorary pallbearers are all who called Iver friend. Chris Hopkins will serve as organist for the service. Pedersen Funeral Home in Morris is in charge of the arrangements.


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I'm harping on learning and using software tools because there are a lot of great hardware devices that could help you. I'm also harping on using your current vendors for adding technology, because as you adopt more cool and new hardware, you want to make sure you're fully integrating with your current tools. The one big "caution" about using technology is this: The more you use, the more your technologies will clash with one another. So try to use all of what you have to its fullest capacity, then integrate new tools as best you can.
Look for New Tools
Now let's take a look at a five cool tools. Some have been around a few years, while others are new. All can take your technology aptitude to a new level.
Your smartphone: Some of your current vendors have apps you can use to make yourself more mobile and efficient. Find out what they have to offer, then browse your app store for other things that might help you. Just a flashlight app could help when cleaning units.
Tablets: If your current PC-based system allows it, you can use a remote log-in service like LogMeIn to do your business as you travel the property. You can do a move-in on the golf cart while showing a unit, and you can bring your apps with you. You can take photos of the unit that's about to go to auction and send or file it on the go. You can load a customer survey and hand it to customers to complete.
Payment terminals: There are stripped-down PCs that can be set up at your counter to take payments. What a great way to add a customer convenience that saves you time on the busy days of the month.
Kiosks: In many markets, self-service move-ins and account management are becoming readily accepted by consumers. Maybe it's time to consider one for your store. A kiosk effectively makes your office open 24/7.
- Automated door locks: If you ever wished there was a way to eliminate the hassle of removing the overlock on doors to accommodate a late-paying customer, think how easy it would be if your management software would know when to slide the automated lock open on a unit as a part of the payment transaction. No more telling people to wait until tomorrow when you have a chance to remove the overlock personally.
Then there are a host of great technologies that are available as a service through websites and package vendors for things like call tracking and monitoring, lead management, reputation management, website analytics, business intelligence, competition analysis, and consumer-market research. It's a whole new wonderful world in which we live. It takes a little adjusting and a lot of learning, but the technology allows us to make storage a passive business for its owners and an enjoyable customer-service mission for its workforce.
Go and ask your superiors now for four or five hours a week to learn about new technologies. Tell them you'll report back with information about all the cool features you can add to your capabilities. You'll run a better business, and your superiors will be happier, too.
Tron Jordheim is the director of PhoneSmart, an off-site sales force serving self-storage owners for more than 10 years. For more information, call 866.639.1715; e-mail firstname.lastname@example.com; visit www.phone-smart.net .


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|Rotating tower bearings
|email@example.com (Chris R. Burger)
|Thu, 10 Oct 1996 10:37:21 +200
I'm in the process of making a 40 m (130') rotating tower. The rotating portion is being made of something similar to 45G. I need to fabricate bearings for the slip rings to run on. Some questions come to mind: * Does anyone have suggestions about suitable bearings? * Are there rollers, made for some other purpose, that would fit the bill? * Should the surface be rubberised, or be bare metal? * Should a bearing be supported on both ends of the axis, or is one end sufficient? Direct replies will be summarised on the Reflector. Thanks Chris R. Burger ZS6EZ -- FAQ on WWW: http://www.contesting.com/towertalkfaq.html Submissions: firstname.lastname@example.com Administrative requests: firstname.lastname@example.com Problems: email@example.com Sponsored by Akorn Access, Inc & KM9P
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This post is part of our FBG Birthday Week celebration! Check out all of the special four-year birthday posts and huge giveaways here!
Last year for our birthday, we shared our thoughts and yours on what it means to be a Fit Bottomed Girl. We also gave a top-10 list of signs that you might be an FBG. This year, we thought we'd mix it up with a fun, interactive fill in the blank. So, we hit up our Facebook page and Twitter to ask readers to complete this phrase: "I knew I was an FBG when ____." The answers? Simply awesome, hilarious and touching.
From Our Facebook Friends
Steve-Becky Kimball: I turned down homemade peanut butter fudge!
Ginger Giannoni: When I achieved my fitness goals and crossed my first finish line.
Fit and Healthy with Beth: You don't want to eat the junk even though you could!
Hardcoremama Fitness with Maria Cappa: People genuinely look shocked to learn my age.
Heather Bosworth Hoe: I lost 100 lbs in a year and ran my first 10K after only trying running 9 months earlier. 🙂
Christian Flamboyant Dart: When I looked in the mirror!
Julia Van de Ven: When dedicating 4% (1 hour) of my day to my fitness became a routine.
Shannon Colavecchio: I embraced my 'junk in the trunk' for the muscles, and how those muscles power me through burpees, jump squats, long cycling climbs, TRX one-legged squats, etc. 🙂
Johanna Lozano: I started keeping a Swiffer by my workout gear to mop up the sweat that soaked the floor every morning.
Rachel Kutskill: My client's sister said "I'll train with you if you can make my butt look like yours!"
Michelle L Thayer: Ran 2.5 miles without breaking a sweat!
Rachel Ailin: I finished my first obstacle race!
Sara Brown: When I fit into a size 2 for the first time since 8th grade! 🙂
From Our Twitter Friends
@tina2086: I wake up earlier than I need to just so I can work out before work.
@MaryJaneSparrow: I started liking to work out.
@gretajacobson: When I baked kale chips for a snack!
@headhaunchos: When my knees quit buckling while trying to squat.
@RoboLikes: When I was more excited for a new pair of sneakers than a new pair of heels 😀
@Hungry_Runner: I knew I was a FBG the day I admitted that I actually LIKE to run!
@rafdarrow: I knew I was a FBG when I rocked the 100 push-up challenge with @denisermt a couple yrs ago!
@Fight4Wellness: I knew I was an FBG when I opted to wear pants rather than a skirt to work to make my midday plank more appropriate.
@JeanneMallory: I put on the pants I bought for inspiration & they were loose in the waist & across my newly fit bottom!
@OnTheGoCooking: I knew I was a FBG when I noticed my butt was back up where it should be! 🙂
We've said it before and we'll say it again, we love you guys. So proud of your fit bottomedness! —Jenn


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Officials with the Lafayette Sheriff's Department tell News 10 that a body has been found in the Benchmark Lounge in Broussard after a fire there.
The identity and cause of death is unknown at this time. Lafayette and Broussard firefighters responded to the call this morning on the 200 block of Tubing Road.
Fire investigators are still trying to determine what caused the fire which also spread to Universal Starters and Alternators.
We will bring you more information as it becomes available.


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Medical billing is one of the fastest-growing employment opportunities in the United States today. Insurance companies, medical offices, hospitals and other health care providers are in great need of trained personnel to create medical claims. This book will ensure learning the skills necessary to become a successful medical claims biller. It is presented in a comprehensive, yet user friendly way, following a logical learning format beginning with a broad base of information and then, step by step, following the course for creation of a medical claim.
This book teaches the skills necessary to become a well-rounded medical biller. By completing this course of study with a satisfactory grade, the user will be granted a certificate and can have the opportunity to work towards an "Honors Certificate", which is even more valuable to a potential employer.


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Fundamentals of Engineering Thermodynamics, Appendices , 7th Edition
112 pages
June 2011, ©2012
This leading text in the field maintains its engaging, readable style while presenting a broader range of applications that motivate engineers to learn the core thermodynamics concepts. Two new coauthors help update the material and integrate engaging, new problems. Throughout the chapters, they focus on the relevance of thermodynamics to modern engineering problems. Many relevant engineering based situations are also presented to help engineers model and solve these problems.
See More
New to This Edition
- Modern and forward-thinking real world applications.
- An increased emphasis on how thermodynamics principles are related to some of the most important issues of today and the coming decade around energy resource use and environmental engineering.
- Integrated coverage of contemporary applications for thermodynamics in the fields of biomedicine and bioengineering.
- New animation-based demonstrations reinforce the concepts in real-world situations.
- Two new coauthors, Daisie Boettner and Margaret Bailey, bring their rich backgrounds of success in teaching and research in thermodynamics to the text.
- Emphasis on energy storage, an area of explosive growth, integrated throughout, including a new introductory section (sec. 2.7), feature on thermal energy storage (chap. 3), followed by a section on energy storage coverage of pumped energy by hydro and compressed storage (sec. 4.8).
- New coverage of the configuration of power plants (chap. 8).
- A wealth of new and revised homework problems (approximately 30%), refreshing the extensive selection of problems in every chapter, organized to help students develop engineering skills in three modes: conceptual, skill building, and design/open ended problems.
- Focus on design concepts, which are interwoven through the book along with a set of newly revised and augmented questions on design and open-ended issues that are part of each set of end of chapter problems.
See More
The Wiley Advantage
- Strong pedagogical structure to enhance student learning, starting each chapter with learning outcomes followed by both in-text and formal examples, then a self-quiz for immediate feedback on understanding. Each chapter ends with a chapter summary to review the topics and prepare for examinations.
- Flexible coverage of application areas in chapters 8-14, including power and refrigeration cycles, psychrometrics, and combustion. Instructors can choose various levels of coverage ranging from short introductions to in-depth studies.
- Class-tested and proven approaches on key thermodynamics concepts, including: the second law of thermodynamics, featuring the entropy balance (Chap. 6) and exergy analysis (Chaps. 7 and 13).
- Integrates the use of computational software tools to enhance problem-solving and to deepen learning by indicating which end of chapter problems are appropriate for these methods.
- Encourages flexibility in the use of units through support for either an SI or mixed SI/English presentation of the course, as well as an emphasis on the systematic application of unit conversion factors.
See More


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Warderick Wells
Warderick Wells is the headquarters of the Exuma Cays Land and Sea Park. The park is a special place to cruisers; many return year after year and contribute financially, and volunteer their services in many ways, serving as park hosts and helping with needed projects. The park is a no take zone by land and sea... which means no fishing, lobstering, conching, or shelling within the park boundaries. The island has mooring balls located near the ranger station in the north field, on the west side of island at Emerald Rock, and on the southeast side of the island at Hog Cay. We moored in the north field several times and at Hog Cay twice during our visits.
The park headquarters, built in 1989, have an office, extensive exhibits of specimens of shells and other items collected in the park, and gift area offering t-shirts, books, charts, ice, and wireless internet for sale. As we climbed the steps to the park ranger's headquarters, the first thing we saw was the spectacular view of the north mooring field. The area is natural harbor and the current runs through and changes direction several times a day with the change of tides.
LuLu had a great time in the mooring field stalking the local birds that came out to visit our boat for tidbits of bread. It brought out her hunting instinct, but fortunately the little bananaquits were smart enough to stay out of her reach! They landed on our solar panels on top of the bimini. Every now and then, a brave one would land on the lifelines in the cockpit. We had to keep an eye on her at all times to make sure she was not able to lay a paw on any of them.
There are lots of great hiking trails criss-crossing the island of Warderick Wells, and we pretty much hiked them all. Good hiking shoes were a must, as the island is pock-marked with holes and sharp limestone.
A favorite location is the hike up to Boo Boo Hill. Boaters have been making the trek to the top of Boo Boo for years.... it is customary for boats to leave driftwood plaques of their boats up there for years. When we visited the park with Pipe muh Bligh, we made plaques and hiked up the hill to add our contributions to the boaters' shrine.
Just to the north of Boo Boo Hill, the trail lead us to the Blow Holes. The blow holes provided a great source of entertainment when our friend Martha McSherry came to visit... the air blowing out of the hole as the waves crashed underneath the island was really strong that day, and blew Martha's hat off! We spent a lot of time laughing and dancing around the blow hole.
All along the Atlantic side of the island, there are stromatolites. They are a living example of the Earth's earliest reefs and form an unusual and special type of reef. Unlike most present-day reefs, which are composed of coral, stromatolites are formed by microorganisms which trap and bind sand grains together and precipitate calcium carbonate to form layered mounds of limestone. Stromatolites are the oldest known macrofossils, dating back over a million years. Geologists and students from universities from all over the world come to this area in the Bahamas to study this unique reef system.
The south mooring field of Warderick Wells is located between Warderick Wells and Hog Cay. There are only five moorings and the beautiful isolated area has great protection from winds from all directions.
There is a deep cut between the islands where we saw eagle rays feeding every afternoon as the tide ripped through.
Ashore, a conch-lined trail through a narrow, palm frond lined path took us to a small opening with a fresh water well, called the Pirate's Lair. In this area grow tall cabbage palms (not indigenous to the Bahamas) and a certain type of grass found only in the Gulf coast areas of Louisiana and nowhere else in the Exumas. In the 1700's, it is believed that it was brought here by pirate ships that used this anchorage.
The Pirate's Lair was used as a meeting place for the pirates when ashore. They would bring their mats and set them up to sit, talk, and recreate, which distributed the seeds of the cabbage palms and the grasses. The ridges of Warderick Wells camouflaged the rigging of the pirate ships while Hog Cay concealed the hull from any ships sailing by offshore. Pirates lying at this anchorage could make easy prey of any vessel passing by heading throughWide Opening channel to Nassau. Martha and I set up hammocks in the lair and read for an afternoon. We got fascinated by all of the birds up in the palm trees and did more bird-watching than reading. Nice relaxing way to spend an day in paradise!
On our trip to Hog Cay in May, we woke up early one morning to see a storm brewing in the distance. We saw waterspouts form in the clouds several miles away and were treated to a spectacular show.
The storm moved away from us and beautiful weather once again descended upon the Cay.
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Tuesday, October 21, 2008
eToys Sale
eToys.com is having a sale on many of their toys. If you have a child that likes dolls, they are selling Bratz (my friend humorously calls them "Prostitots") for $5 and Hannah Montana dolls for $6.99. They also have Fisher Price toys 20-66% off. Here are numerous other deals they have going.
2 comments:
- Michelle said...
OH, I have to laugh - Prostitots is hilarious!!! And appropriate...
- October 21, 2008 at 9:59 AM
- Daffernia said...
- This comment has been removed by the author.
- November 13, 2008 at 3:49 AM
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bottom line. We're excited to be there."
Marsch has yet to appear for the Fire in an Open Cup match this season, though he is likely to be a force in the midfield in Kansas City. Another midfield general that could return to the Fire lineup is captain Chris Armas. He is ahead of schedule in his rehabilitation process after a knee operation barely three weeks ago.
"(Armas) is coming along very well," said Sarachan. "We hope this is a week where he can get back, whether it's Wednesday or Saturday. We're very pleased on that end."
The return of Armas could do nothing but help the Fire's quest for success, both in the Open Cup and in league play. With only four games remaining in the MLS season, grabbing a championship could be the catalyst to propel the Fire into the MLS Cup Playoffs. Chicago has never missed an MLS postseason in club history, and getting a taste of that championship feeling could be just what their young side needs to keep that streak alive.
"I don't think it saves your season, but it certainly helps in a lot of ways," said Marsch. "I think it will help with confidence. It will already help us knowing that we have on in the bank, and now we can throw everything out there and give our best effort to win the second. Any year you win an Open Cup, you're having a successful year."
Jonathan Nierman is a contributor to MLSnet.com. This story was not subject to the approval of Major League Soccer or its clubs.


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Australian Cinematographer provides a balance of feature articles from all areas of the cinematography industry since our first issue over 10 years ago, in June 1998.
The magazine is produced by a team of professionals and cinematographers, both working and retired. This team's background is from a broad range of the industry, covering all genres of cinematography.
Our regular contributors come from a range of industry backgrounds, suppliers to post production and our own members.
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