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The Twin City Tavern hugged the Missouri state line just west of Kansas City's famed Westport district; walk across the two-lane road to use the ATM and you're in Kansas. It was his dream place, a spot where he could finally put the accent on the "grill" and dish out his homemade chili, signature sandwiches, spaghetti with my Italian mother's sauce, thick burgers, steaks and even fresh salads. His claim to fame was his Friday-night shrimp boil. He had shrimp brought up from Louisiana each week and boiled them in big stockpots roiling with cheap white wine and Boulevard Pale Ale, along with new potatoes and corn on the cob. The beer-and-wine boil was typical; most folks never knew the difference, but he loved that kind of little detail. He enjoyed expressing himself through the food and its presentation, even if it was being served up in a corner joint.
I get the sense Tom Gullickson feels the same way, even if he isn't flipping burgers and boiling shrimp in the tiny kitchen at Griffins Farmer's Market Café in Soulard. For six years Gullickson ran McMurphy's Grill at St. Patrick's Center. After that he bought into Nadine's but recently sold his interest. Griffins owner Robert Howe brought in Gullickson about two months ago, giving him free rein to create an atmosphere and tweak the menu of the year-old operation, which is located in a 100-year-old building that has housed a restaurant and bar since just after Prohibition.
728 Lafayette Ave.
St. Louis, MO 63104-3818
Category: Restaurant > American
Region: St. Louis - Soulard
614 N. 11th St.
St. Louis, MO 63101
Category: Restaurant > American
Region: St. Louis - Downtown
314-436-7705. Hours: 11 a.m.-10 p.m. Tue.-Fri.; 2-10 p.m. Sat.; 2-8 p.m. Sun. Brunch 9 a.m.-2 p.m. Sat.-Sun. Call for bar hours.
I ate at Griffins when it opened. It wasn't bad -- kind of a "not bad for what it is" type of place, but that's not atypical for a casual Soulard restaurant. And that's the challenge for Gullickson: How do you successfully blend restaurant fare beyond burgers and fries into what's mostly a bar? Gullickson says he envisions more café and less grill. "I like the word café," he says. "This summer, when we have the tables out front, we'll feel like a café."
He says his goal is to change the quality of the food and test the market based on what customers say they want. Enter Rene Cruz, known simply as Chef Rene. Gullickson hired the young cook from Nadine's because he liked his pastas and sauces and because he considers Cruz, whose résumé includes graduation from the Cordon Bleu Culinary School in Minneapolis and five years as a corporate trainer, "one of the best soup makers." Together the duo has revamped the menu twice since Mardi Gras, indicating that things are still being tinkered with. (Note to Dad: They dropped the spiced boiled shrimp!) A few recent visits suggest that some nurturing still needs to take place.
In keeping with Soulard's New Orleans "Cre-jun" theme -- i.e., the blending of Cajun and Creole -- Cruz's entrées center on sauces and spices. A basic puttanesca pasta -- one of the simplest, most rustic dishes imaginable -- is braced, as expected, with red and green bell peppers, capers, onions and olives. But mix all that in a very light, subtly spiced cream sauce and you've got something to linger over. The three decorative strands of dry noodles poked into the dish as an accent exhibit a flair beyond bar-and-grill -- it's something Dad might have done if he didn't think his patrons would have laughed out loud.
Chicken wings and strips are workaday bar-and-grill appetizers. Herbed tomato bruschetta, spinach-artichoke dip and Creole catfish fingers, not so common. A choice of three quesadillas round out the list of starters, including one stuffed with tomatoes, mushrooms and Monterey Jack cheese on top of that flavorful spinach-artichoke dip (the other two quesadillas: chicken and cheese). And true to Gullickson's claim, Cruz's soups are worth slurping. Typically, you can select from three special soups of the day, plus the daily vegetarian chili. On one visit I tried the Cuban lentil -- chunks of beef simmered in a rich broth of lentils and spices, brightened by the fresh taste of cilantro. Paired with one of Griffins' salads, a bowl of the Cuban soup would make for a good lunch.
Griffins is a tomato's throw away from Soulard Market, so it's fitting that Cruz expanded the salad selection from Cobb and Caesar to include spinach and Greek. Come summer, he says, there'll be an even greater variety of fresh fruits and salads. Meantime, he's tweaked the dressings, infusing them with Asian, Italian and Mediterranean influences (you might request some extra pineapple-feta ranch to dip your bread in). But a wedge salad special -- that thick hunk of iceberg that's showing up on more and more local menus -- suffered from heavy-handed drenching of bleu cheese. And what's with the boxed croutons on the dinner salad?
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P311 is an 8-kDa intracellular protein that is highly conserved across species and is expressed in the nervous system as well as in vascular and visceral smooth muscle cells. P311-null (P311–/–) mice display learning and memory defects, but alterations in their vasculature have not been previously described. Here we report that P311–/– mice are markedly hypotensive with accompanying defects in vascular tone and VSMC contractility. Functional abnormalities in P311–/– mice resulted from decreased total and active levels of TGF-β1, TGF-β2, and TGF-β3 that arise as a specific consequence of decreased translation. Vascular hypofunctionality was fully rescued in vitro and in vivo by exogenous TGF-β1–TGF-β3. Conversely, P311-transgenic (P311TG) mice had elevated levels of TGF-β1–TGF-β3 and subsequent hypertension. Consistent with findings attained in mouse models, arteries recovered from hypertensive human patients displayed increased P311 expression. Thus, we identified P311 as the first protein known to modulate TGF-β translation and the first pan-regulator of TGF-β expression under steady-state conditions. Together, our findings point to P311 as a critical blood pressure regulator and establish a potential link between P311 expression and the development of hypertensive disease.
P311 is an 8-kDa intracellular protein that is highly conserved across species and is normally expressed in the nervous system and in vascular and visceral smooth muscle beds. In addition, P311 is detected in myofibroblasts (1), at the invading edge of glioblastomas (2), in regenerating nerve and lung (3, 4), and in hypertrophic scars (5). P311 has been implicated in myofibroblast differentiation as well as nerve and lung regeneration (3, 4). Although it neither belongs to any established protein family nor possesses signature motifs that suggest function, P311 features a conserved PEST (rich in proline [P], glutamic acid [D], aspartic acid [E], and serine [S] or threonine [T])-like amino acid sequence at the N terminus (6). PEST motifs were originally identified in short-lived proteins as targets for ubiquitin-proteasome degradation (7) and subsequently found to mediate protein-protein interactions and activation (8–14). Although deletion of P311 in mice results in no overt phenotype (15), P311–/– mice display learning and memory defects, consistent with the presence of P311 in the nervous system (15, 16).
TGF-βs are multifunctional growth factors capable of inducing a spectrum of cellular events, including proliferation, cell cycle arrest, differentiation, programmed cell death, and stimulation of matrix deposition (17–19). TGF-βs are synthesized as a large homodimeric precursor (pro–TGF-β) that is cleaved into mature TGF-β and latent-associated protein (LAP), which remain noncovalently associated (20, 21). Before TGF-βs can exert their biological effects, they must dissociate from LAP in order to become active (20, 21). Active TGF-βs signal through TGF-β receptors I and II and the transcriptional coregulators Smad2 and Smad3 (22–24). Upon phosphorylation (i.e., activation), Smad2 and Smad3 bind to Smad4, translocate to the nucleus, and bind to the CAGA box (found in the promoters of multiple TGF-β–responsive genes; refs. 25, 26) to activate their transcription (22–24). Smad-independent pathways had been also identified (22, 23).
Because P311 is also expressed at high levels in VSMCs (1, 6), we explored its potential role within the systemic vasculature. Here, we found that P311–/– mice were markedly hypotensive, with accompanying defects in vascular tone and VSMC contractility. Functional abnormalities in P311–/– mice resulted from decreased translation of TGF-β, which decreased the level and activity of TGF-βs. Conversely, mice overexpressing P311 showed an elevation in level and activity of TGF-βs as well as systemic hypertension. Consistent with these findings, arteries from hypertensive humans displayed increased P311 expression. In summary, our studies identified P311 as the first regulator of TGF-βs translation with a critical role in blood pressure control.
Western blot analysis and immunohistochemistry (IHC) confirmed the presence of P311 in mouse and human VSMCs and its absence in the endothelium and vasculature of P311–/– mice (Supplemental Figure 1, A–D; supplemental material available online with this article; doi: 10.1172/JCI69884DS1). P311 expression levels were higher in arteries than in veins (Supplemental Figure 1D). Morphometry did not show differences between P311–/– and WT mice (Supplemental Figure 1, E and F). Telemetric determination revealed diurnal systolic and diastolic blood pressures to be 16.5 ± 3 and 14 ± 5 mmHg lower, respectively, in P311–/– mice than in WT mice, with slightly increased nocturnal differences (Figure (Figure1A).1A). Echocardiographic studies performed in conscious mice revealed enlarged aortic diameter in P311–/– animals that disappeared under general anesthesia (Figure (Figure1B).1B). There were no significant differences in other echocardiographic parameters, except for increased cardiac output (Supplemental Figure 2). Together, these findings suggested a decrease in myogenic tone, which was confirmed by pressure myography using resistance arteries (~150 μm in diameter) (Figure (Figure1C1C and Supplemental Figure 3). Myographic studies on isolated aortas showed decreased contractility in response to K+ depolarization in P311–/– mice (Figure (Figure1E).1E). Consistently, P311–/– resistance arteries also showed decreased contractility in response to K+ and to vasoconstriction agonists (norepinephrine, phenylephrine, epinephrine, and angiotensin II), with no difference in the vasodilatation response to hydralazine (Figure (Figure1E1E and Supplemental Figure 4, A–E). P311–/– aortas demonstrated decreased RhoA activity, as assessed by RhoA-GTP levels, as well as the phosphorylated fraction of MYPT1 (Figure (Figure1F).1F). Collagen gel contraction assays showed that VSMCs isolated from P311–/– aortas were less efficient in contracting collagen gels than those derived from WT animals, but their contraction improved after P311 transfection (Figure (Figure1,1, G and H).
Although real-time PCR demonstrated upregulated Tgfb1, Tgfb2, and Tgfb3 mRNA levels in aortic tissues isolated from P311–/– mice, ELISA showed that total and active protein levels of the 3 isoforms were severely decreased in tissue extracts and in plasma samples from P311–/– mice (Figure (Figure2,2, A–C). Immunoblot analyses demonstrated reduced expression of pro–TGF-β1, pro–TGF-β2, pro–TGF-β3, and LAP-1 (Figure (Figure2D).2D). We found that blocking TGF-β activity resulted in a decrease in the contractile response of WT and P311–/– mouse–derived resistance arteries. This decrease was statistically significant only in the WT arteries, which had more TGF-β than their P311–/– counterparts (Figure (Figure2E).2E). VSMCs cultures also showed increased Tgfb1, Tgfb2, and Tgfb3 mRNA levels, while protein levels were decreased (Supplemental Figure 5, A and B). Consistent with these findings, phosphorylation of the transcriptional coregulators Smad2 and Smad3 was also decreased (Figure (Figure2F).2F). Mice carrying an active TGF-β reporter construct, CAGA12/GFP, showed lower activity in P311–/– versus P311+/+ animals (Figure (Figure2G).2G). P311–/– VSMCs isolated from CAGA12/GFP-transgenic mouse aortas also showed a loss of TGF-β activity relative to WT controls (Supplemental Figure 5C).
The increase in TGF-β mRNAs, combined with the decrease in TGF-β isoform levels, suggested that P311 regulates TGF-β translation, degradation, or both. Since we previously found that P311 binds to LAP (6), we first considered the possibility that P311 is involved in TGF-β degradation through the engagement of its PEST domain. Ubiquitin immunoprecipitation assays showed no differences in ubiquitin-bound TGF-β between aortas from P311–/– and WT mice (Supplemental Figure 6). Luciferase untranslated region (UTR) expression vectors, including the 5′- and 3′-UTRs of TGF-β1, TGF-β2, or TGF-β3 (Figure (Figure3A),3A), demonstrated increased translation in P311–/–-derived VSMCs transfected with P311 compared with empty vector control (Figure (Figure3B).3B). Further analyses demonstrated that the stimulatory effect of P311 on luciferase expression was confined to the 5′-UTR of the respective TGF-β isoforms (Figure (Figure3B).3B). RNA immunoprecipitation revealed enrichment of TGF-β 5′-UTR mRNAs in P311–/–-derived VSMCs transfected with P311 compared with sham-transfected VSMCs and other controls (Figure (Figure33C).
In rescue experiments, P311–/– and WT mice were treated with a combination of TGF-β1, TGF-β2, and TGF-β3 (referred to herein as TGF-β1-3), delivered intraperitoneally at a dosage sufficient to correct the decrease in plasma levels of active TGF-β observed in P311–/– mice (Figure (Figure4A).4A). TGF-β1-3 administration restored blood pressure as well as vascular tone, contractility, and RhoA activity in P311–/– mice (Figure (Figure4,4, B–E). Over a period of 10 days, TGF-β supplementation induced comparable hypertensive responses in P311–/– and WT mice, as determined by plethysmography (Figure (Figure4B),4B), despite TGF-β1-3 in plasma reaching higher levels in WT mice (Figure (Figure4A).4A). Collagen gel contraction assays showed restoration of contractility in P311–/– VSMCs after TGF-β1-3 treatment (Figure (Figure4F).4F). When administered individually, TGF-β1 and TGF-β3 exerted effects comparable to those observed with TGF-β1-3 (albeit less pronounced in magnitude), whereas TGF-β2 had no effect (Supplemental Figures 7–9).
P311-transgenic (P311TG) mice exhibited increased levels in all 3 pro–TGF-βs in aortic tissues, resulting in increased plasma levels of total and active TGF-β1, TGF-β2, and TGF-β3 (Figure (Figure5,5, A and B). Increased TGF-β activity was also confirmed in CAGA12/GFP reporter mice (Figure (Figure5C).5C). Consistent with the increased TGF-β expression levels and activity, P311TG mice developed systolic and diastolic hypertension, as determined by plethysmography (Figure (Figure55D).
P311 levels were assessed in arterial tissue recovered from normotensive and hypertensive patients. Real-time PCR showed increased P311 mRNA levels in aortic tissues from hypertensive males relative to sex-matched normotensive controls (Figure (Figure6A).6A). In addition, IHC analyses demonstrated higher P311 protein levels in both arteries and arterioles from hypertensive males compared with normotensive controls (Figure (Figure6B).6B). Consistent with these findings, TGF-β levels were increased in arteries from hypertensive patients compared with normotensive controls, and so were the nuclear levels of Smad2 and Smad3 (Figure (Figure6,6, C and D), indicative of increased TGF-β activity.
P311 is a highly conserved, 8-kDa intracellular protein abundantly expressed in the nervous system and in VSMCs and visceral smooth muscle cells with roles in myofibroblast transformation, cell migration, and tissue regeneration. Deletion of P311 in mice results in no overt phenotype (15). However, consistent with a functional role for P311 in the brain, these P311–/– mice display learning and memory defects (15, 16). Since P311 is also expressed at high levels in VSMCs, we explored its potential role within the systemic vasculature.
Western blot analysis and IHC confirmed the presence of P311 in mouse and human vascular muscle and its absence in the vasculature of P311–/– mice. Furthermore, IHC indicated that P311 expression was higher in arteries than in veins. Gross examination and morphometry demonstrated normal blood vessel organization and histological architecture in P311–/– mice; however, echocardiographic studies performed in conscious mice revealed an enlarged aortic diameter that disappeared under general anesthesia, a finding that suggests, among other things, a decrease in myogenic tone. Consistent with such a possibility, P311–/– animals displayed significant systemic hypotension. These changes were intrinsic to the vascular smooth muscle, rather than a result of P311 lacking in the nervous system, since aortas and resistance arteries isolated from P311–/– mice demonstrated hypocontractility in response to various vasoconstriction agonists. RhoA activity, a critical determinant of blood pressure and vascular muscle contractility (27), was also reduced in P311–/– aortas. Consistent with the fact that active RhoA promotes vascular muscle contraction by inhibiting myosin light chain phosphatase (MLCP; via ROCK-mediated phosphorylation of its regulatory subunit, MYPT1) (28), the phosphorylated fraction of MYPT1 was decreased in P311–/– mice. Finally, VSMCs isolated from P311–/– aortas were less efficient in contracting collagen gels than those derived from WT animals, while contraction improved after P311 transfection, confirming that the functional abnormality rested on the vascular muscle itself and that P311 directly regulated VSMC contractility.
We and others have reported that P311 modulates TGF-β expression when transfected into NIH-3T3 fibroblasts (1, 5, 6). Thus, we next determined the expression of TGF-β1, TGF-β2, and TGF-β3 in P311–/– and WT aortas. Interestingly, while Tgfb1, Tgfb2, and Tgfb3 mRNA levels were upregulated in aortic tissues isolated from P311–/– mice, total and active protein levels of the 3 isoforms were severely decreased in VSMCs as well as in plasma samples of these mice. The reduced TGF-β activity occurred at the level of pro–TGF-β1, pro–TGF-β2, and pro–TGF-β3 expression, with accompanying decreases in the corresponding levels of LAP, which noncovalently associates with mature TGF-β. Consistent with these findings, downstream targets of TGF-β signaling, (i.e., the phosphorylated transcriptional coregulators Smad2 and Smad3) were also decreased. Furthermore, P311–/– mice carrying an active TGF-β reporter construct, CAGA12/GFP, confirmed lower activity than their WT counterparts in whole aortas and in VSMC cultures. These results differed from our previous observations with NIH-3T3 cells, in which P311 transfection abrogated TGF-β1 and TGF-β2 expression without affecting TGF-β3 expression (6). The observation that NIH-3T3 cells and VSMCs responded differently to P311 suggests that its effect is cell specific, a possibility further supported by a prior observation that P311 overexpression stimulates TGF-β1 transcription in dermal fibroblast cultures (5). Our in vivo findings, however, were inconsistent with a role for P311 in TGF-β transcription by VSMCs.
Remarkably, TGF-β1-3 administration alone restored blood pressure, contractility, and RhoA activity in P311–/– mice. In a similar fashion, contractility was also restored in P311–/– VSMCs after treatment with the TGF-β1-3 cocktail. When administered individually, TGF-β1 and TGF-β3 exerted effects comparable to those observed with TGF-β1-3 (albeit less pronounced), whereas TGF-β2 had no effect. While prior studies demonstrated a role for TGF-β1 in blood pressure regulation (29–31), this represents the first instance in which the potential effect of TGF-β2 and TGF-β3 in blood pressure levels was assessed and the first demonstration that TGF-β3 increased them.
To determine whether P311 can directly regulate TGF-β activity and vascular tone in vivo, we generated transgenic mice overexpressing P311. As predicted, P311 transgenic mice exhibited an increase in all 3 pro–TGF-β levels in aortic tissues, with increased TGF-β activity — as indicated by the CAGA12/GFP reporter mice — resulting in increased plasma levels of total and active TGF-β1, TGF-β2, and TGF-β3, as recorded for human hypertension and TGF-β1 (32–34). Furthermore, the P311 transgenic mice developed hypertension, which indicates not only that P311 is needed to prevent hypotension, but that its increase is sufficient to cause high blood pressure.
The increase in TGF-β mRNAs in P311–/– mice, combined with the decrease in TGF-β isoforms observed, suggests that P311 regulates TGF-β at the posttranscriptional level, acting at translation, degradation, or both. Ubiquitin immunoprecipitation assays ruled out differences in degradation. However, when luciferase expression vectors were constructed that included the 5′ and 3′-UTRs of TGF-β1, TGF-β2 or TGF-β3, the luciferase protein was expressed at lower levels in P311–/– versus WT cells, which indicates that P311 regulates translation of TGF-βs. Further analyses demonstrated that the stimulatory effect of P311 on luciferase expression was confined to the 5′-UTR of the respective TGF-β isoforms. In addition, RNA immunoprecipitation revealed enrichment of the TGF-β 5′-UTR mRNAs in VSMCs isolated from P311-transfected P311–/– mice compared with sham-transfected controls, consistent with a role for P311 in translation of TGF-βs. Since P311 has no RNA-binding motifs, the P311-mRNA interaction is likely to be indirect through one or more yet-uncharacterized proteins. Hence, P311 controls TGF-β levels and/or activity by acting as the first known regulator of its translational activity.
As P311 had not been previously linked to blood vessel homeostasis, we finally considered the possibility that the protein plays a role in human hypertension. We assessed P311 levels in arterial tissue recovered from normotensive and hypertensive patients. Indeed, increased P311 mRNA levels were detected in aortic tissues from hypertensive males relative to sex-matched normotensive controls. In addition, IHC analyses confirmed higher P311 protein levels in both arteries and arterioles from hypertensive versus normotensive tissue. Although our studies showed that increased P311 level per se led to hypertension, it is possible that the high P311 expression detected in arteries of hypertensive patients is, in part, the result of increased mechanical stress, since in previous studies we found that mechanical tension induces P311 in embryonic mesenchymal cells (1). Taken together, these data support the conclusion that P311 plays a heretofore unrealized role in modulating hypertensive responses in humans.
TGF-β is known to act as a critical effector of blood pressure regulation (29–31). To date, however, the pathophysiologic control of TGF-β–dependent vascular tone has largely been confined to angiotensin II, whose action is in great part mediated by TGF-β (35–38) and TGF-β1 polymorphisms (39–42). Herein, we identified P311 as a previously unrecognized major regulator of the TGF-β–vascular tone axis. In the absence of P311, total and active levels of TGF-β1, TGF-β2, and TGF-β3 decreased in vascular muscle and plasma, in tandem with decreased RhoA activity and increased MLCP activity, resulting in low vascular contractility, tone, and hypotension. These abnormalities were intrinsic to the vascular muscle, as opposed to resulting from lack of P311 in the nervous system. In contrast, mice overexpressing P311 featured increased production of TGF-βs in the vascular musculature and increased circulating levels of TGF-β1, TGF-β2, and TGF-β3 as well as TGF-β activity in vivo, while displaying a hypertensive phenotype. These data, combined with the observed linkage of increased mRNA and protein levels of P311 in hypertensive humans, served to identify P311 as a new and potentially important effector of blood pressure regulation.
Generation of P311–/– mice (C57BL/6 mice with deletion of the entire P311 coding region on both alleles) was described previously (15). For in vivo determination of TGF-β activity, transgenic mice were generated by crossing CAGA12/GFP animals (carrying a TGF-β–responsive promoter element CAGA12 upstream of GFP; provided by H.C. Dietz, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA) with WT (P311+/+) or P311–/– animals. TGF-β activation in reporter mouse tissues was histologically visualized by IHC with an Ab against GFP (Abcam). For P311 overexpression, transgenic mice were created by using pBROAD3 vector (InvivoGen) under the control of ROSA26 promoter. The P311TG line was selected by real-time PCR of P311 and used for further breeding. 4-month-old males were used in this study, and age-matched WT C57BL/6 mice (Charles River Laboratories) were used as controls. Animals were housed at the University of Chicago animal facility (20°C~25°C and 12-hour light cycle) and supplied with rodent diet no. 2918 (18% protein, 6% fat and moderate phytoestrogen; Harlan Laboratories).
Aortas and first-branch mesenteric arteries were dissected from the mice, and the attached fat and soft tissues were trimmed under a microdissecting microscope. The dissected blood vessels were immediately used for experiments or frozen at –80°C until use. For real-time PCR, samples of abdominal aorta, right below the diaphragm, from 5 normotensive male patients and 5 hypertensive male patients (age 60 ± 3 years) were collected from autopsies within 4 hours postmortem. For IHC, paraffin blocks from surgically removed, uncomplicated hernia sacs from 18 normotensive male patients and 21 hypertensive male patients (age 60 ± 3 years) were selected from the Department of Pathology archival material. In all cases, the history of hypertension was 5 ± 2 years, blood pressure values at the time of diagnoses were 100 ± 5 over 150 ± 5, and all had a record of poor treatment compliance. None of the patients had past or present history of additional illnesses.
TA11PA-C10 telemetry devices (Data Sciences International) were implanted subcutaneously along the flanks of 8 P311–/– mice and 8 WT controls for chronic acquisition of blood pressure parameters and heart rate. The devices' catheters were placed with the tip at least 2 mm into the aortic arch. Data from WT and P311–/– mice were collected for a 1-week period and analyzed using Dataquest A.R.T. software (supplied by Data Sciences International).
Plethysmographic blood pressure was recorded using an 8-channel CODA noninvasive blood pressure acquisition system (Kent Scientific) following the manufacturer's protocol. Mice were placed in a clear acrylic restrainer with a built-in nose cone for at least 30 minutes prior to obtaining pressure measurements. Systolic, diastolic, and mean blood pressure as well as heart rate were recorded. Blood pressures were monitored on days 0, 3, 6, and 10 of TGF-β treatment studies.
Transthoracic echocardiography was performed in awake and anesthetized mice using a Doppler system (Acuson c256) equipped with a 15-MHz linear transducer (15L-8) (43). The heart was first imaged in the 2D mode in the parasternal long-axis view, for measurement of wall thickness and chamber dimensions as well as aortic dimension. LV cross-sectional area at end-diastole and -systole were measured on a 2D short-axis view of the papillary muscles. The following parameters were also obtained: (a) LV chamber dimensions; (b) LV wall thickness; (c) LV mass (LVM); (d) LV ejection fraction (LVEF); (e) shortening fraction; (f) cardiac output; and (g) aortic dimensions.
Mice were intraperitoneally injected with recombinant (r) human TGF-β1, rTGF-β2, rTGF-β3, or rTGF-β1-3 (R&D Systems). Injections were given to mice once daily for 10 days at a dose of 250 ng (rTGF-β1, rTGF-β2, and rTGF-β3) or 100 ng of each (rTGF-β1-3). Before and after rTGF-β treatments, blood pressure was monitored, and echocardiography was performed (only for combined rTGF-β1-3 treatment). After 10 days of treatment, aortas were isolated for myography studies, along with Western blot analysis or ELISA (see below).
Thoracic aortas and mesenteric resistance arteries were cut into rings approximately 2 mm in length, and contractility was measured with a DMT 610M multi-myograph system (DMT-USA Inc.). Optimal tension was initially applied, and tissues were allowed to equilibrate for 1 hour in 5 ml physiological salt solution (PSS; containing 118.99 mM NaCl, 25 mM NaHCO3, 4.69 mM KCl, 1.18 mM KH2PO4, 1.17 mM MgSO4, 2.5 mM CaCl2, 0.03 mM EDTA, and 5.5 mM glucose) at 37°C, gently pumped with a gas mixture of 95% O2 and 5% CO2. For TGF-β receptor inhibitor treatment, PSS containing 100 μM LY364947 (Sigma-Aldrich) was used. Aortic and arterial contractions were determined after sequential addition of KCl, vasoconstrictors (norepinephrine, phenylephrine, epinephrine, and angiotensin II; Sigma-Aldrich), or vasodilator (hydralazine; Sigma-Aldrich) to PSS buffer.
Mesenteric resistance arteries (100–150 μm in diameter) were dissected in PSS buffer and mounted on a DMT 110P pressure myograph system (DMT-USA Inc.). Myogenic tone was assessed by subjecting the arteries to a series of pressure steps (10–125 mmHg), and lumen diameters were recorded. Active and passive diameters were determined in PSS buffer (containing 2.5 mM CaC12) or Ca2+-free PSS buffer (containing 2 mM EGTA instead), respectively. Myogenic tone was calculated as percent constriction relative to the passive lumen diameter at each respective transmural pressure: ([diameterpassive – diameteractive]/diameterpassive) × 100. An intermediate pressure (75 mmHg) was used to determine the response of arteries to K+.
GTP-bound (i.e., active) RhoA was isolated from aortas using a commercial kit (Millipore). Aortas from WT and P311–/– mice were lysed with Rho-binding lysis buffer (50 mM Tris, pH 7.2, 1% Triton X-100, 0.5% sodium deoxycholate, 0.1% SDS, 500 mM NaCl, 10 mM MgCl2 with 10 μg/ml leupeptin, 10 μg/ml aprotinin, and 1 mM PMSF). Lysates were clarified by centrifugation, and active RhoA was precipitated with agarose beads conjugated with 20 μg of a GST-tagged fusion protein corresponding to residues 7~89 of mouse rhotekin Rho-binding domain. Precipitates were subjected to immunoblotting with RhoA Ab supplied in the kit. Aorta lysates incubated with 100 μM GTPγS and 1 mM GDP were used as positive and negative controls, respectively.
Dissected aorta and mesenteric arteries from WT and P311–/– mice were formalin fixed and paraffin embedded. 5-μm aorta sections were stained with DAPI nuclear dye (5 μg/ml in water) for 10 minutes and observed under a Zeiss Axioplan microscope equipped with epifluorescence optics. For each field, 2 images were acquired by a Leica DC500 digital camera to visualize elastic lamina (autofluorescence observed in the fluorescein channel) and nuclei (observed using a UV filter set). The images were then overlapped using Leica IM 1000 Image Manager software. The length of the innermost elastic lamina (IEL) and the number of nuclei comprised between two elastic laminas in the aorta, and between internal and external elastic lamina in the mesenteric arteries were determined using Metamorph software (version 7.5; Molecular Devices).
ELISAs were performed using Emax Immuno assay system (Promega) with modified protocols on fresh aortic tissues and serum. TGF-β1 mAb (supplied in the kit), TGF-β2 mAb (MAB612; R&D Systems), and TGF-β3 mAb (MAB643; R&D Systems) were coated on a 96-well plate and incubated overnight at 4°C. After blocking, TGF-β protein standards and acidified or nonacidified serum samples (to show total or active TGF-βs, respectively) were allowed to bind at room temperature for 1.5 hours. Secondary Abs — TGF-β1 polyclonal Ab (pAb) (supplied in the kit), TGF-β2 pAb (BAF302; R&D Systems), and TGF-β3 pAb (BAF243; R&D Systems) — were added to complete the sandwich, followed by the chromogenic substrate 3,3′,5,5′-tetramethyl benzidine (TMB), stop solution (1 N HCl), and recording of absorbance at 450 nm.
IHC was performed at the University of Chicago Pathology Core Facility. The immunoperoxidase procedure was applied to formalin-fixed, paraffin-embedded aortas from WT and P311–/– mice and formalin-fixed, paraffin-embedded human tissues. 5-μm tissue sections were incubated with anti-mouse P311 Ab (1:50 dilution; ref. 44), anti-human P311 Ab (1:50 dilution; ref. 45), anti–TGF-β1-3 Ab (1:20 dilution; MAB1835; R&D Systems) or anti-Smad2/3 Ab (1:50 dilution; sc-6033; Santa Cruz) after antigen unmasking by boiling in fresh citrate buffer, and reactions were developed with Vectastain ABC kit (Vector Laboratories). Intensity quantifications were performed in human artery muscular layer at 6 equidistant points. IHC figures were converted to 8-bit images, and densitometry was conducted using Image J (version 1.41x; NIH).
Isolated aortas were denuded of adventitial layer by microdissection and of endothelial cells by passing through a sterile pipette tip and kept in Fungizone solution (Invitrogen) for 2~3 min. The aortas were then cut into small pieces and incubated in 100 μl of collagenase II enzyme solution (1.5 mg/ml) at 37°C for 5 hours. The VSMCs were then released from the digested tissues by pipetting up and down through a tip. The released cells were washed three times in PBS, resuspended in culture medium DMEM with 10% FBS and seeded onto plates. VSMCs were used at passage 1.
RNA isolation and cDNA synthesis were done with aortic tissues and cultured aortic VSMCs using TRIzol (Invitrogen) and iScript cDNA synthesis kit (Bio-Rad). Real-time PCR for mouse cDNA was conducted using iQ SYBR Green Supermix (Bio-Rad) and the following primers: Tgfb1 sense, 5′-TGAGTGGCTGTCTTTTGACG-3′; Tgfb1 antisense, 5′-TTCTCTGTGGAGCTGAAGCA-3′; Tgfb2 sense, 5′-GTGACATGGACAGTGGATGC-3′; Tgfb2 antisense, 5′-GCGGACGATTCTGAAGTAGG-3′; Tgfb3 sense, 5′-TGGAGTCATGGCTGTAACT-3′; Tgfb3 antisense, 5′-CACTCACACTGGCAAGTAGT-3′; Gapdh sense, 5′-ATCACCATCTTCCAGGAGCGA-3′; Gapdh antisense, 5′-GCCAGTGAGCTTCCCGTTCA-3′. For detection of P311 mRNA from human aortas, the following primers were used: sense, 5′-TCCAAACAAGGACATGGAGGG-3′; antisense, 5′-AGGTAACTGATTCTTGGGGAG-3′.
For transient transfections, VSMCs at approximately 70% confluence were transfected with the P311 expression construct pCMV-Myc-P311 (Clontech) using Lipofectamine 2000 reagent in Opti-MEM (Invitrogen). At 24 hours after transfection, cells were trypsinized and used for gel contraction studies (see below). For reporter assay, TGF-β1-3 5′- and 3′-UTR regions were cloned into pGL3-promoter firefly luciferase vector (Promega) to generate reporter constructs. P311–/– mouse VSMCs were plated on 6-well plates and transfected with the P311 expression vector, the reporter constructs, and renilla luciferase internal control vector pRL-SV40. 48 hours after cotransfection, the Dual-Luciferase Reporter Assay System (Promega) was used to determine the ratio of firefly/renilla luciferase activity, as indicated by the manufacturer.
48 hours after transfection with the P311 expression construct pCMV-Myc-P311 or empty vector, cells were lysed in lysis buffer (25 mM Tris, 150 mM NaCl, 1 mM EDTA, 1% NP-40, 5% glycerol, pH 7.4) supplied with Halt Protease Inhibitor Cocktail (Thermo Scientific). Cell lysates were subject to immunoprecipitation using anti–c-Myc agarose (A7470; Sigma-Aldrich). Agarose beads were washed 3 times in lysis buffer and resuspended in TRIzol for RNA isolation. Coimmunoprecipitated RNAs were detected by real-time PCR using primers specific to Tgfb1 (sense, 5′-GCTCCCCTATTTAAGAACACCC-3′; antisense, 5′-TTGAGGTTGAGGGAGAAAGC-3′), Tgfb2 (sense, 5′-AGTGGGAGAGAAAGAGAGAAGG-3′; antisense, 5′-GCGACCCTAAAATAGACCTCTG-3′), Tgfb3 (sense, 5′-AAGAGAAGCAAGGGACAGAAG-3′; antisense, 5′-GCTGGGATGAGGGATTATGTAC-3′), Inhba (sense, 5′-TGACAAAACAGAAGGGACCC-3′; antisense, 5′-CAGCAAAAGTCGTGTGGTTG-3′), B9d2 (sense, 5′-ACAGTGCACCTTGGTATCG-3′; antisense, 5′-ACAGTCTCCAGAGTCCACG-3′), Actb (sense, 5′-CTGTATTCCCCTCCATCGTG-3′; antisense, 5′-GCCTCGTCACCCACATAG-3′), and Tuba1a (sense, 5′-GCGAAGCAGCAACCATG-3′; antisense, 5′-TCTTGTCACTTGGCATCTGG-3′).
Gel-contraction studies were conducted using 5 ml of rat tail collagen I solution (2 mg/ml in 0.1% acetic acid) mixed with 1 ml of 10× DMEM and 1 ml of 0.1 N NaOH to neutralize the pH before adding 3 ml of trypsinized VSMCs (WT, P311–/–, and P311 expression vector–transfected P311–/–; 3 × 105 cells/ml) in culture medium. The mixed collagen gel solution was casted in 60-mm culture plastic dishes (4 ml/dish). After incubation at 37°C for 30 minutes, polymerized gels were detached and covered with 4 ml DMEM with 10% FBS. Lattices were photographed after 7 days, and magnitudes of gel contraction were calculated. For treatment purposes, the polymerized gels were incubated with regular media containing rTGF-β1, rTGF-β2, rTGF-β3, or rTGF-β1-3 at a concentration of 10 ng/ml.
Aorta lysates and cultured aortic VSMC lysates (20 μg total protein) were resolved on SDS-PAGE gels and transferred onto nitrocellulose membranes (BioRad) for immunoblotting analysis. Abs against P311 (44, 45), TGF-βs, LAP-1 (R&D Systems), c-Myc (Sigma-Aldrich), MYPT1 (Cell Signaling Technology), phospho-MYPT1 (T696; Santa Cruz), and GAPDH (Santa Cruz) were used to detect target proteins. An ECL Plus Western blotting detection system (GE Healthcare) was used for detecting the chemiluminescence signal.
All experiments were repeated at least 3 times, and data are shown as mean ± SD. Differences between 2 groups and treatments were determined by 1-way ANOVA or by 2-tailed Student's t test. A P value of 0.05 or less was considered statistically significant.
All animal procedures performed herein were approved by the University of Chicago IACUC in accordance with NIH guidelines. All protocols for human tissues were approved by the University of Chicago IRB according to NIH guidelines. All human tissues were obtained from the Human Tissue Resource Center at the University of Chicago (and therefore have deidentifiers); patient informed consent was not required.
We thank Harry C. Dietz for providing CAGA12/GFP transgenic mice and Yee Wong for excellent technical assistance in the performance of pressure myograph studies. This work was supported by NHLBI grants HL-48730, HL-77514, and HL-78752 to L. Schuger. K.R. Badri is an American Lung Association Interstitial Lung Disease Scholar (Dalsemer Research Award; DA-196629-N).
Conflict of interest: The authors have declared that no conflict of interest exists.
Note regarding evaluation of this manuscript: Manuscripts authored by scientists associated with Duke University, The University of North Carolina at Chapel Hill, Duke-NUS, and the Sanford-Burnham Medical Research Institute are handled not by members of the editorial board but rather by the science editors, who consult with selected external editors and reviewers.
Citation for this article: J Clin Invest. 2013;123(10):4502–4512. doi:10.1172/JCI69884.
Kameswara Rao Badri's present address is: Office of Sponsored Research Administration, Savannah State University, Savannah, Georgia, USA.
PubMed Central Canada is a service of the Canadian Institutes of Health Research (CIHR) working in partnership with the National Research Council's Canada Institute for Scientific and Technical Information in cooperation with the National Center for Biotechnology Information at the U.S. National Library of Medicine(NCBI/NLM). It includes content provided to the PubMed Central International archive by participating publishers.

subset: commoncrawl


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Steve Ybarra: Here is the question of the day: Will Democrats have the guts to call out the Republicants and tell America it is time to say yes? Yes to education, yes to job creation, yes to bringing our troops home, yes to cutting military spending, yes to new energy policy, yes to ending hatred.
While the Oil Gushes
Tina Dupuy: The BP spill exposed that we're still commuting in eight-cylinder singly occupied vehicles, hopped up on plastic goods and scoffing at high-speed rail projects. Our government is representative – we haven't clamored to get off oil. If anything we've threatened to riot for having to pay too much at the pump.
The Oil Next Time
A Growing Sense of Anger at Obama – and Others
I'm so angry I feel like concealing a loaded hand gun and walking into a national park. No, I'm not going postal. Once President Obama signs the new credit card law, it will be legal for anyone to march around Yellowstone packing heat just for the fun of it. Although it's usually angry, bitter, little […]
Specter Dumps GOP; Few Rats Remain on Sinking GOP Ship
Arlen Specter's stunning announcement that he is changing parties to become a Democrat is merely the latest example of the how the Republic Party is losing its grip on America. "Since my election in 1980 as part of the Reagan Big Tent, the Republican Party has moved far to the right," Specter tells reporters, not […]


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At last. Michelangelo Antonioni is an Italian director who has just made his seventh film and who is so highly esteemed abroad that there has already been an Antonioni Festival in London. For the eleven years of his career no Antonioni film has been released here. Now at last comes L'Avventura, which is the sixth of his works. The first ten minutes make it clear that this is the work of a discerning, troubled, uniquely gifted artist who speaks to us through the refined center of his art.
Educated Americans are eager customers for national self-analysis, especially for studies which compare the present unfavorably to the past. They Hock to writers like Vance Packard, who see America in the throes of a decline in individualism, thrift, culture and other long-prized virtues. One of the favorite topics of the decline-and-fall school of social analysis is the homogenization of American life.
For nearly 20 months a subcommittee of the Senate Committee on the Judiciary has been holding hearings, ostensibly on "the Communist threat to the United States through the Caribbean," presided over by James O. Eastland of Mississippi. He is assisted by Senators Dodd, Johnston of South Carolina, McClellan, Ervin, Hruska, Dirksen, Keating and Cotton. How many witnesses have been called has not been disclosed. The testimony of only a few has been released, and that has been edited before publication.
Arthur Miller, in his plays, has done some representative worrying for all of us about certain defects and defeats in contemporary life. Now he has broken a five-year silence with a screenplay called The Misfits in which he expresses further concern. The premise is promising: a Chicago girl goes to Reno for a divorce, and there meets three Western men. She is desperate for reliable human relationships, they are in a last-ditch fight against the diminution of large-scale life.
The President-elect may not, in every instance, have picked "the best men available" for his Cabinet, but since "the best man," like "the very best butter," is a matter of personal taste, the new appointees and John Kennedy should be given the benefit of a few doubts. On the whole, the Cabinet has a new-minted brightness. There are doubts, nevertheless, and the Defense appointment gives rise to the most important of them. Robert S.
As they do with governments, countries usually get the film stars they deserve. Marilyn Monroe and Sophia Loren, each of whom now appears in a film comedy well-tailored for her, are good examples. To see both in one week, as I did, is inescapably to compare them not only as women and actresses but as national evocations.
As they do with governments, countries usually get the film stars they deserve. Marilyn Monroe and Sophia Loren, each of whom now appears in a film comedy well-tailored for her, are good examples. To see both in one week, as I did, is inescapably to compare them not only as women and actresses but as national evocations. Although each lady has a big international audience, each seems to represent what her compatriots, male and female, consider desirable in woman.
Invitation to a Beheading By Vladimir Nabokov Translated by Dmitri Nabokov (Putnam's; $3.95) In his autobiography, Conclusive Evidence, Vladimir Nabokov devotes a few pages to discussing the emigre Russian writers whom he knew in Berlin and Paris before 1939: Bunin, Poplavski, Rodasevich, "But," he goes on, Normal 0 false false false MicrosoftInternetExplorer4 st1\:*{behavior:url(#ieooui) } /* Style Definitions */ table.MsoNormalTable {mso-style-name:"Table Normal"; mso-tstyle-rowband-size:0; mso-tstyle-colband-size:0; mso-style-noshow:yes; mso-style-parent:""; mso-padd
The Mansion By William Faulkner (Random House, $4.75) The Snopeses have always been there. No sooner did Faulkner come upon his central subject—how the corruption of the homeland, staining its best sons, left them without standards or defense—than Snopesism followed inexorably. Almost anyone can detect the Snopeses, but describing them is very hard. The usual reference to "amorality," while accurate, is not sufficiently distinctive and by itself does not allow us to place them, as they should be placed, in a historical moment.


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Founder of Aikido (39): The Reestablishment of The Aikikai Foundation
by Kisshomaru Ueshiba
Aiki News #68 (August 1985)
(The following is a chapter summary printed with the kind permission of Mr. Kisshomaru Ueshiba, Aikido Doshu, based on the original Japanese text published in 1977.)
August 15, 1945, the day the war ended, was truly a shock for the Japanese. We were fully convinced that this was the end of aikido. However, the Founder was silently at work on the Aiki-En farm in Iwama. Whenever I spoke to him, he just said, "aikido won't be destroyed. It has a bright future before it." Although he became much thinner as a result of the serious illness he suffered and which even endangered his life, he showed no sign of weakness when breaking the ground with a hoe. By his manner he seemed to laugh at those who were panic-stricken.
Iwama and the Aiki Shrine
The Aiki Shrine was nearly completed when the war broke out. The Founder looked very satisfied and said, "Now, the inner shrine of aiki has been completed." He looked relieved as if years of burden were lifted from his shoulders.
"First, we will establish the true purpose of aikido by creating a link between man and god. This shrine represents the starting point for the attainment of this goal. What is necessary now is to commune with nature to our utmost," were the words the Founder murmured as if to convince himself.
At the beginning in Iwama, there was only an outdoor dojo in the corner of the farm. However, since there were many requests from students in the neighborhood and Tokyo, a practice dojo of 36 tsubo (about 560 square feet) was built. This dojo, the predecessor of the Ibaraki Dojo (now headed by Morihiro Saito Sensei), was probably completed in the summer of 1945, the year the war ended, and its existence turned out to be a significant factor during the confusion following the war. When the war ended, the Tokyo dojo was opened up to some thirty families who were burnt out during the air raids. Thus, the seat of aikido was temporarily transferred to this dojo in Iwama (about 3 years).
Transfer of Headquarters to Iwama
This partially unavoidable transfer of control offered several advantages. Apart from my personal elation over being able to live with the Founder for the first time in many years, we could for example continue our training as much as we liked without worrying about the eyes of the US Occupation Army. This situation also played a major role in sustaining the line of family succession in aikido because many eager young people from neighboring villages gathered together in Iwama. It also provided those old deshi who were demobilized from the battlefront with a place of recreation and relaxation. It helped them to raise their morale in order to re-enter into society.
Things in Iwama proceeded this way for about two years after the war. However, gradually this group came to want to practice regularly even if in only on a modest scale. Also, they were prepared to do anything to startup Aikido again. Although I thought it might be a bit premature, I was urged on by both old and young students. I decided to revive aikido in the forefront of the budo movement.
Revival of Aikido
I occasionally went to the 12-mat room in the dojo in Tokyo from Iwama and started to prepare a draft for the necessary paperwork. I asked Mr. Kinya Fujita and Mr. Katsuzo Nishi for their advice and also discussed the matter with the new students entering the dojo. I kept the Founder informed of the situation whenever I returned to Iwama. However, he would tell me to do whatever I liked and always adopted the attitude of an observer. According to what my mother told me in her later years, the Founder appeared very pleased that his son was at last beginning to take aikido seriously.
(The full article is available for subscribers.)


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Senior sociology major Nicole Manglona Torres was recently named a 2010 Truman Scholar, a competitive national award that recognizes students who exhibit exceptional leadership potential and a commitment to careers in public service.
Torres' extensive community service includes volunteering at Glide Memorial Church, where she helps San Francisco's poor and homeless, tutoring Oakland high school students, and serving as co-president of the USF club San Quentin Alliance for C.H.A.N.G.E., a student group that seeks to help incarcerated men assimilate back into their communities as constructive and productive members of society. Torres did all this while maintaining an A grade-point average.
"Since coming to USF, Nicole has distinguished herself as one of the most talented students in the College (of Arts and Sciences) and the university as a whole," said Patrick Murphy, politics professor and Truman Scholar faculty sponsor to Torres.
The award, given by the Harry S. Truman Scholarship Foundation to about 60 students nationwide, carries with it a scholarship worth up to $30,000 for graduate study. Torres plans to use it to attend law school, eventually returning to her native Saipan (part of the United States Commonwealth of the Northern Mariana Islands in the Pacific Ocean) to work in the public defender's office.


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I had no idea what he was talking about. I don't know many
people men or women who enjoy being controlled. "What do you mean?" I asked.
Right Now already thinks he is your Mr. Right so if you make some adjustments and you think it's worth making then go ahead because this is one guy who will not let you down. All women want to know if their man is Mr. Right. They must have made bad choices in the past so they want to know if the man they are currently dating is worth their commitment.
I felt the same way during my own separation. I could barely pull myself out
of bed each morning and then I would see him looking happy and carefree. It made me feel quite rejected and depressed. And frankly it caused me to participate in behaviors that made things worse for us. So I do have unique insights about this which may help you.
It's a tricky business I know! 3.) Get a life! You don't have to ditch your friends just because you got a txt from him saying he's available. Men fall for independent and self-sufficient women. Make sure you give time to other aspects of your life like your job family how do you tell a man you like him friends and hobbies. It's Signs He Is Unhappy In His Marriage perfectly alright to text or call a guy first once in a while but don't overdo it that he might Signs He Is Unhappy In His Marriage best advice on long distance relationships think you are crazy.
Ideally they would like to play the field for as long as possible (while also having someone to cook and care for them) and then settle down when they have no other advice to women from men choice. Learning how to get a man to commit earlier rather than later is something that a lot of women are trying to do. It has always been a struggle to get a man to commit to anything more than casual dating and some men won't even go that far.
Reply but don't jump and do it instantly let him wait. You are a busy girl right? You aren't just sitting around waiting on him to call or text. Meet him with wit and humor but some healthy resistance. If you can end the conversation first all the better.
I was actually close to being engaged to one of them but I didn't go through with it because she couldn't control me. But my wife Christine* could. If I wanted to go out with my friends she'd say 'Have fun' and that was it. It was such a change from the other girls I dated who used to give me a hard time wanted to know where I was going and why they couldn't come with me.
When you talk to your guy friends you will see that learning how to get a man to commit will likely depend on the kind of guy that you are dating how long you have been together and the kind of life you already have. You never want to get married because you connived your way into making him propose to you or you tricked him somehow into thinking that he would lose you if he didn't commit. Ideally you would like a man who is willing to commit without any pressure from you.
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But infection risks are much higher if there are more than one or two sexual partners involved. If you must have multiple sexual partners you'd at the very least be advised to use barrier protection such as that which is offered by condoms. The second strategy through which you can avoid having to deal with the nastier effects of HPV would be by seeing to it that you keep your immunity in tip top condition.
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Q: Who is most likely to capture the Democratic presidential nomination?
Democrats (88 votes)
Now 3/8/08 Hillary Rodham Clinton 17 percent 46 percent Barack Obama 82 percent 53 percent Neither (volunteered) 1 percent 1 percente>
"Tough as nails, determined, and just keeps going. If you were not impressed by her before, you should be now."
"If she keeps winning most contests, the supers will tip it to her because she is a better bet in November."
"She has answered a few fundamental questions: Who is tougher? Who has been better vetted? And finally, who would the Republicans prefer to run against? It isn't Hillary any longer."ADVERTISEMENT
"Still has the delegate count and the war chest."
"Democrats will not take the nomination away from Sen. Obama and risk the long-term alienation of a generation of younger voters and destroy the party's political bond with African-American voters."
"Barring a complete collapse in Indiana, he'll have the delegates needed to win and avoid erosion of his expanding superdelegates."
"He continues to have a substantial lead in delegates and the popular vote. He's heading into better states, and he'll maintain those leads. Hillary has become unelectable nationally against McCain."
"It looks like Obama, in no small part because the media has so skewed the numbers. According to the pundits, if Obama is ahead in the eighth inning, we should call the game and not let the superdelegates have their turn at bat. It is bizarre."
"HRC cannot win the nomination at this point. All she can do is prolong the agony—hers and ours—and help McCain along the way."
"Sooner or later reality will sink into Camp Clinton that she can't win on pledged delegates; and a nomination based on superdelegates' overriding pledged delegates is a doomed nomination."
"Clinton's win in Pennsylvania nets her a whopping 10 delegates—it's over."
"All she has left in order to win is to keep moving the goalposts and make the case that she wins the 'big' states or the 'critical' states. It is just not a good enough argument for the superdelegates to give her the nomination, unless they want civil war and a sure loss in November and clearly they don't."
"I could say more here but am too angry. The narcissism of the Clintons has become near-pathological. They cannot win but can only continue to do damage."
Republicans (89 votes)Now 3/8/08 Hillary Rodham Clinton 17 percent 50 percent Barack Obama 80 percent 46 percent Neither (volunteered) 3 percent 4 percent e>
"With superdelegates, Obama may have the numbers, but it's now mostly a game of public relations. If he has become 'just another politician' in the eyes of Democrat voters, they will choose Hillary because at least they know what they are getting."
"Clinton will continue to hang in there, hoping for another Obama misstep or nuclear meltdown to scare the down-ballot superdelegates into joining her."
"She won [Pennsylvania] and can make the argument to the superdelegates that Obama can't win in the fall. His numbers will begin to fall under her barrage of attack ads. I am assuming she'll have the money to stay in the race."
"Will win Indiana and Puerto Rico, an indication that her coalition is broader than his."
"In my heart, I feel that the Clintons are like vampires, somehow always able to rise from the dead. But I can't see how the numbers allow them to get there. So I'm sticking with the O-man."
"The superdelegates know that if he isn't nominated the party will blow up."
"The Democrats are having buyers' remorse, but it's too late to turn back now."
"Hillary's only remaining option is to win North Carolina and Indiana, and her scorched-earth policy is making enemies."
"I'm beginning to have my doubts that he can hold on, but
I think the Democratic Party will implode if Hillary pulls this thing out."
"The guy is like Reagan in two ways—golden tongue, Teflon skin."
"Time, money, and numbers are in his favor: It's too late to beat him."
"The party will close the deal for him; a deal he hasn't shown an ability to close himself."
"She can still steal it from him, but each day, each primary result, each negative attack against Obama renders that a less likely outcome."
Q: Which Democratic presidential candidate would do better against John McCain in November?
Democrats (88 votes)Hillary Rodham Clinton 45 percent Barack Obama 50 percent Both (volunteered) 5 percent e>
"There is no stature gap between HRC and McCain, and she's battle-tested and ready."
"She has now made the case, ably assisted by Obama himself, that Obama cannot consolidate the broader Democratic coalition necessary to beat McCain."
"With her, there would be no surprises. She's been thoroughly tested. Obama remains untested, and Republicans will not hesitate to espouse and exploit unanswered questions about his relationships and experience."
"If the election is about the economy, she can hark back to the '90s. If it is about security, she can be against the war but still look tough."
"She appeals more than Obama does to the voters who will decide the race."
"While Clinton has done better than Obama with working-class voters in a Democratic primary, a general election is completely different. Obama still has the potential to expand the electorate in ways that Clinton cannot."
"I think Obama reflects the future of the party and where we need to go. With Clinton we fight the last election."
"HRC is simply too intensely disliked by too many people, fair or not. And we have seen the damage that can be done by her spouse."
"He is the only candidate who can and has expanded the electorate by a significant number."
"There is no joy in this assessment. We are caught between two flawed options—a fighter with impossibly high negatives, and a jazz singer who can't find the right tune for True Grit America. And so we may lose the race that just six months ago appeared to be in the bag."
Republicans (89 votes)Hillary Rodham Clinton 55 percent Barack Obama 42 percent Both (volunteered) 3 percent e>
"She has less 'risk' on legislative and association angles for Republicans to capitalize on."
"If she is nominated, Missouri, Kentucky, West Virginia, and Tennessee are all in play. If he is nominated, McCain wins all of them."
"She never gives up."
"I used to think that Clinton would be an easier general matchup for McCain, because she is a polarizing figure that would fire up our base. But in recent weeks Obama has shown his true extreme-left colors, which won't play in Macomb County, Michigan."
"She has the gender advantage that's built into the general election now, plus the toughness of a pure political fighter."
"She keeps all the 'bitter' people in the fold."
"He has the ability to make history in a way that would have a lot more people rooting for him than Hillary, without turning off one-quarter of the Dem base."
"Obama draws a sharper contrast in a year with an unpopular war, a troubled economy, and a GOP president with record-setting negatives."
"Obama, half-dead and brutalized, has less baggage than Sen. Clinton."
"Hillary's voters will back Obama; Obama's voters will hate Hillary. And Obama's age and crossover appeal is a better match against McCain."
"While Obama might offer McCain a chance to pick up more Reagan Democrats, McCain would still prefer Clinton due to her vast, enduring unfavorables."
"She can't get to 50 percent plus one: too much baggage, too much entrenched dislike, too much resistance to another presidential dynasty."
Democratic Political Insiders
Karen Ackerman, Jill Alper, David Axelrod, Brad Bannon, Dave Beattie, Andy Bechhoefer, Cornell Belcher, Mitchell W. Berger, Mike Berman, Donna Brazile, Mark Brewer, Ed Bruley, George Bruno, Deb Callahan, Bonnie Campbell, Bill Carrick, Martin J. Chavez, Tony Coelho, Jim Craig, Jerry Crawford, Stephanie Cutter, Jeff Danielson, Jim Demers, Tad Devine, Debbie Dingell, Monica Dixon, Michael Donilon, Tom Donilon, Anita Dunn, Jeff Eller, Steve Elmendorf, Carter Eskew, Eric Eve, Vic Fazio, Peter Fenn, Scott Ferson, Gordon Fischer, Tina Flournoy, Don Foley, Don Fowler, Gina Glantz, Joe Grandmaison, Anna Greenberg, Stan Greenberg, Pat Griffin, Michael Gronstal, Marcia Hale, Paul Harstad, Laura Hartigan, Mike Henry, Leo Hindery, Jr., Harold Ickes, Marcus Jadotte, John Jameson, Steve Jarding, Jonathon Jones, Jim Jordan, Gale Kaufman, Shar Knutson, Kam Kuwata, Celinda Lake, David Lang, Sylvia Larsen, Jeff Link, Bill Lynch, Steve Marchand, Jim Margolis, Paul Maslin, Terry McAuliffe, Caroline McCarley, Susan McCue, Gerald McEntee, Tom McMahon, Phil McNamara, David Medina, Mark Mellman, John Merrigan, Steve Murphy, Janet Napolitano, David Nassar, Marcia Nichols, John Norris, Tom Ochs, Tom O'Donnell, Scott Parven, Jeffrey Peck, Debora Pignatelli, John Podesta, Tony Podesta, Bruce Reed, Mame Reiley, Steve Ricchetti, Susan Rice, Will Robinson, Steve Rosenthal, David Rudd, John Ryan, Wendy Sherman, Terry Shumaker, Bob Slagle, Erik Smith, Doug Sosnik, Darry Sragow, Karl Struble, Katrina Swett, Sarah Swisher, Eric Tabor, Jeffrey Trammell, Ed Turlington, Mike Veon, Rick Wiener, Bridgette Williams, and JoDee Winterhof, Jim Zogby.
GOP Political Insiders
Dan Allen, Stan Anderson, Gary Andres, Saulius (Saul) Anuzis, Rich Ashooh, Whit Ayres, Brett Bader, Mitch Bainwol, Gary Bauer, David Beckwith, Wayne Berman, Charlie Black, Kirk Blalock, Carmine Boal, Jeff Boeyink, Ron Bonjean, Jeff Buley, Luke Byars, Nick Calio, Danny Carroll, Ron Christie, Jim Cicconi, Cesar Conda, Jake Corman, Greg Crist, Diane Crookham-Johnson, Fergus Cullen, Rick Davis, Mike Dennehy, Ken Duberstein, Steve Duprey, Debi Durham, Frank Fahrenkopf, John Feehery, Don Fierce, Carl Forti, Alex Gage, Sam Geduldig, Benjamin Ginsberg, David Girard-diCarlo, Bill Greener, Jonathan Grella, Lanny Griffith, Janet Mullins Grissom, Doug Gross, Todd Harris, Steve Hart, Christopher Healy, Ralph Hellmann, Chris Henick, Terry Holt, David Iannelli, Clark Judge, David Keating, David Kensinger, Bruce Keough, Bob Kjellander, Ed Kutler, Chris Lacivita, Jim Lake, Chuck Larson, Steve Lombardo, Joel Maiola, Gary Maloney, David Marin, Mary Matalin, Dan Mattoon, Bill McInturff, Mark McKinnon, Kyle McSlarrow, Ken Mehlman, Jim Merrill, Mike Murphy, Phil Musser, Ron Nehring, Terry Nelson, Neil Newhouse, David Norcross, Ziad Ojakli, Jack Oliver, Van B. Poole, Tom Rath, Scott Reed, David Rehr, Steve Roberts, Jason Roe, David Roederer, Ed Rogers, Dan Schnur, Russ Schriefer, Rich Schwarm, Brent Seaborn, Rick Shelby, Andrew Shore, Don Sipple, Robin Smith, Javier Soto, Fred Steeper, Bob Stevenson, Eric Tanenblatt, Heath Thompson, Jay Timmons, Warren Tompkins, Ted Van Der Meid, Dirk van Dongen, Jan van Lohuizen, Dick Wadhams, John Weaver, Tom Wilson, Dave Winston, Ginny Wolfe, and Fred Wszolek.
This article appears in the April 26, 2008 edition of National Journal Magazine Contents.


text:
The title of the new Pirates film has been announced - Pirates of the Caribbean: On Stranger Tides
Let the discussion begin!
The title of the new Pirates film has been announced - Pirates of the Caribbean: On Stranger Tides
Let the discussion begin!
Last edited by Dustysage; 01-18-2011 at 10:38 AM.
What the?! How could I have missed this!! I am sooooooooo angry that I was not there!! I cannot believe it... this has put me in a depressed funk to be sure!! Any pictures or video from this one?
OK, well, back on topic... I am excited for Pirates 4. I am a tad concerned about the "Stranger Tides" thing. How strange is strange? I hate it when special effects etc overpower the story. There is so much potential with the pirates storyline and I love the relationship between Captain Jack and Barbossa. So, definitely can't wait till 2011!!
Ugh!! can't believe I missed that....
What I'm wondering is, if the premier will be at Disneyland, are we gonna crash Micechat like last time?
I got to admit, i was very much on the fence with another Pirates film, but I just cant resist. Cant wait
Heeerre's Johnny!
Johnny's entrance at the D23 expo:
YouTube - Johnny Depp as Captain Jack Sparrow at the Disney D23 Expo
Last edited by Dustysage; 01-18-2011 at 10:39 AM.
Thanks for the video Barbossa! Who doesn't love that man!
OH MY GOSH!! I am absolutely speechless of that video!! What I wouldn't give to have been there to see that. I did already see him at Comic Con, but to see him in person as Captain Jack, I would have died where I stood.
By the way, not too keen on the new Pirates movie title, but super excited for the movie!
I'm on the fence for a 4th as well, but I'll try to remain optomistic till an actual summary and cast listing are released. I know a lot of people weren't happy with DMC and AWE (personally, I enjoyed it myself.), so I wonder how successful they really plan it to be.
I'm DEFINETELY on board if Geoffrey Rush returns. Jack Sparrow is fun, but Barbossa is my favorite.
Oh dear. Another one. I love the idea of Pirates, and I love the first movie, but I confess I'm getting tired of this series. :/
I just don't see why it deserves so many movies....Yeah. This will quickly become a very long rant, so I'll stop now.
I heard rumors that Zac Efron was hired on for this one.
He might have to do a magical Kraken Dance to get it to awake from it's slumber lol
Stranger tides? that is a weird strange last name title.


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Shoeb K. Zainuddin
Indonesia's property market is undergoing a massive transformation as the economy expands and a rising middle class demands better housing.
Some people are hunting for high-rise apartments in Central Jakarta, others for sprawling housing estates in Bekasi, Tangerang and Bogor, but either way, demand for property is growing fast, and many of the largest developers are responding with a building spree.
Demand for condominiums remained buoyant in the first quarter this year due to low interest rates, property experts say. And while sales in proposed projects declined slightly, they still hit a strong 2,039 units. The bulk of these sales were outside the central business district, which accounted for 67.1 percent of the quarter's total sales.
Residential property prices have spiked along with the rising demand.
"In Jakarta, prices have gone up by 30 to 40 percent cumulatively over the past three years," said Luke Rowe, a senior technical adviser at Jones Lang LaSalle, a real estate services firm.
Indonesians have fueled much of the push for property, but Rowe said the market would fare much better if foreigners were allowed to participate, as they can in Malaysia, Singapore and Australia.
"All three [other] countries have experienced strong growth in their property markets over the past few years by opening up to foreign ownership," he said. "Malaysia's second home policy, for example, has significantly broadened the country's property market."
Foreign ownership of Indonesian property has been widely debated but little progress has been made. Still, under the current system, some foreigners can buy land and buildings. Specifically, expatriates with work permits can use the Hak Pakai (right to use) land title, which grants the exclusive right to use land and any buildings on it.
The Hak Pakai title is valid for an initial term of 25 years but can be extended twice — for 20 years and then another 25 years. Titleholders may sell at any time during this period. When buying property, they should be Indonesian residents at the time of purchase.
"This is an attractive opportunity and many expatriates living in Indonesia have been active using this title," Rowe said.
With it, expatriates possess legal standing and can take out a mortgage from some banks. Commonwealth Bank of Australia is the first foreign bank focused on extending mortgage loans to foreigners based in Indonesia.
These loans are known as consumption loans, and to qualify for them, expatriates need to have an Indonesian tax filing number and an active working permit, including either a KITAS temporary stay permit or a KITAP stay permit.
However, property sector experts say the Hak Pakai title has a flaw: It is not appropriate for the vast majority of apartment projects. That's because at the time of construction, most developers opt for Hak Guna Bangunan (right to build) as the underlying land title, which is more acceptable to Indonesian buyers.
Although there has been some talk of amending the laws for land titles, it seems unlikely anything will change before the elections in 2014. For now, most nonresident foreigners cannot participate in the property market here because they cannot get a Hak Pakai title. Some, however, may have other options: they can use an Indonesian nominee or they can form a foreign investment company, which must have a purpose beyond owning real estate.
The most critical point, Rowe said, is that the property law system recognizes the legal certainty associated with leases.
"A lessee does not necessarily have to register a 'registered lease' because lease-holding over a property implies primary beneficial use rights until the expiry of such a lease," he said.
This allows foreigners to take long-term leases on property, especially if the lease includes an option to purchase, which would be triggered in the event that laws regarding foreign ownership are adjusted in the future.


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General [Richard] Myers [Vice Chairman, Joint Chiefs of Staff] and Secretary Cohen, thank you both for those very, very kind words.
Secretary Cohen, Aristotle once observed that the highest vocation was to serve the community. Throughout your service to this nation you have guided our men and women in uniform with the greatest of care and skill. So I am honored by the confidence you and the President have placed in me, and I pledge myself again to this highest of vocations. Thank you for your confidence in me.
Janet Cohen, the first lady of the Department of Defense, has been so helpful to me in terms of working the issues so critical to our men and women. She talks the talk. She walks the walk, and she makes a difference. Janet, please stand up, thank you very, very much. [Applause.]
Anne, Kerry and Libby, as always, thank you for being here. Also, I want to welcome my cousin, Mary Lou de Leon, who is a professor of Nursing at the University of Washington
Also, I would be remiss if I did not recognize long-term friends [General] Joe [Supreme Allied Commander Europe, designate] and Dede Ralston who are here. There is no surprise that in a younger life I wanted to be an astronaut. So one of the great heroes in my life was John Glenn. Another was the first American to walk in space, an astronaut named Ed White. He was killed on the way to the moon, but when I look at Joe Ralston everyday I see those same characteristics of a man who can push the envelope, have the Right Stuff, be an incredible gentlemen and a perfect leader for our times. Thank you for being here, and if you would please stand. [Applause.]
When Senator [Strom] Thurmond, an advocate for our Junior ROTC, took me to Columbia, South Carolina, there were those in the department who had questions about the program. But he took us there that day and we became believers. I think today on this parade field we have seen the young high school students from South Carolina with their discipline, with their commitment, and with their skills. Senator Thurmond, we are thankful to you for opening that door because with your leadership, and with the commitment of Secretary Cohen, we have expanded the Junior ROTC program much more broadly in our country, and we thank you for that. Please stand. [Applause.]
Former Congressman Sonny Montgomery and the other key congressional representatives who are here, you are the great pillars behind our people in uniform, without whom they would not be the fine force that they are. So thank you for being here.
Deputy Secretary Talbott, who is really helping to shape a new world, we thank you for being here today. [Applause.]
[Former] Deputy Secretary [of Defense John] Hamre; Service Secretaries and Chiefs, Members of the Armed Forces, and defense leaders, an extraordinary team of friends and remarkable public servants; distinguished guests; thank you for all being here today.
It has been said that "in a brief space, the generations change and, like runners, pass on the torches of life." Today, in this brief space, we are graced with three generations that reveal the purpose of our lives.
Among us are members of that Greatest Generation, our friends from the Soldiers' and Airmen's Home here in Washington who, a half century ago, quite literally saved the world from tyranny. They are Americans like John Tuggle, who survived the sinking of his PT boat and then waged guerilla warfare throughout occupied Philippines until its liberation; Mary Tropeano, who was there as a young sergeant for the preparations for D-Day and, later, for the liberation of Europe; Fay Steele, who earned 13 Air Medals and a Bronze Star for his valor in combat on a B-26 bomber; and John Wright, who fought in both World War II and Korea as a member of the legendary Buffalo Soldiers. To all the veterans who are here, for your sacrifices in war and for shaping a America in peace, I would ask that you stand so that we might honor your service. [Applause.] You are heroes of the 20th Century and we thank you for being with us.
Also joining us, as Secretary Cohen and General Myers mentioned, are members of the next generation of leaders, our Junior ROTC friends from South Carolina, who I first met on a trip to several high schools Columbia with Senator Thurmond. I invited them here because they are true models for their peers, driven by dedication and personal responsibility. They are young people of great optimism who give us great hope for our country. So again, we thank you, as we thank the Active Duty honor guards of the Military District of Washington, for inspiring us this morning.
These two generations, of yesterday and tomorrow, speak to us today, to our generation. For at the end of the day when those who walk the path of public service ask, "Why do we serve?" These inspiring Americans remind us of the answer. We serve to preserve the gifts of freedom we have received from those who came before. We serve to pass on these gifts to those who will come after.
Perhaps no one bears this burden more than our soldiers, sailors, airmen, Marines and Coast Guardsmen, Active Duty, Guard and Reserve. I am inspired by their power and professionalism wherever I go. Whether on a Bosnian mountaintop, Mount Viz, at the time commanded by General [Ric] Shinseki [now Chief of Staff, United States Army], overlooking a valley made safe by their service; in the mud of Macedonia the night before they rolled north to bring peace to Kosovo; or at bases and communities across this country, such as last weekend in the wind, snow and sunshine of Alaska. And so whether we pass on to the next generation the gifts of freedom passed to us rests on whether we remain true to these men and women in uniform who preserve freedom in our time.
So, as an institution, we need to continue caring for our greatest treasure, our people. They ask nothing more than a sound quality of life – health care, housing and fair treatment -- for themselves and for their families. They deserve nothing less.
We need to ensure that our forces can prevail in any mission. So we need to strike that balance between readiness and modernization, the readiness that allows our military to meet the diverse challenges of the present, and the modernization that puts in their hands the tools and technologies they need to survive in the future.
At the same time, we need to continue the work of Secretary Cohen and Dr. Hamre prepare this department for the new threats of this new world: strengthening our defenses, our computers against terrorists in cyberspace, and our nation against those with weapons of mass destruction; ensuring that in this global economy our industry partners remain vibrant and that we can share critical technologies with friends while securing our capabilities from foes, and I thank Secretary Talbott and Jim Steinberg, the Deputy National Security Advisor, for their work in this critical area Finally, we also need to continue reforming our business practices so that our operations are as agile and efficient as the force they support.
Of course, none of this will be possible if we succumb to narrow interests rather than the national interest. So we also take occasions such as these to renew our dedication to the highest ideals of public service, of service on behalf of people, the brave and talented people in uniform who look to us for support.
So the three generations on this parade ground remind us why we serve as individuals. These abiding goals remind us where we must go as an institution. Yet, the question remains. How? To what inner spirit do we turn for strength and for guidance?
More than half a century ago, President Franklin Roosevelt offered the answer. Even as he led that Greatest Generation through the darkest Depression in our country's history, even as he guided them through the deadliest war in human history, even as he lay near his deathbed in Warm Springs, he still held high hopes for this nation. He said in those hours, "The only limit to our realization of tomorrow will be our doubts about today. Let us move forward with strong and active faith, faith in our God who gives us strength every day, faith in our families who are there to share the burdens with us, and faith in our country and in ourselves."
Ladies and gentlemen, members of the armed forces, to stand before you as Deputy Secretary is a great honor. And so, with no doubt in our purpose or our people, I pledge to you, as we do to each other, to embrace that role of the runner and to accept and pass on that torch of life and liberty and to endeavor to move this great institution forward with strong and active faith.
Secretary Cohen, I thank you for your confidence. Ladies and gentlemen, thank you very much. [Applause and standing ovation.]


text:
Dinner & Cruise with Fireworks
Watch the biggest fireworks show of the year
- on 20th August from our ship!
The 20th of August is a national holiday in Hungary. We are celebrating the foundation of the state, and our first christian king, St. Stephen, while it is also the holiday of the "new bread". This is the biggest celebration in Hungary! Our special Firework Cruise features a welcome champagne, delicious warm buffet dinner, live gipsy and Hungarian music and unlimited drink consumption. After dinner you can also admire the biggest event of the year from the upper deck of the ship, in a real close-up!
The Panorama of Budapest is not only an unforgettable experience, but an illustration of the capital's history. The banks - added to the World Heritage List of UNESCO - offer one of the world's most outstandingly beautiful urban cityscapes. The site, insribed in 1987, streches from the Chain Bridge to the Technical University on the Buda side; an area containing the Gellért Baths, the Gellért Hill with the Statue of Liberty and the Citadel, furthermore the building ensemble of the Buda Castle.
The delicious meals on the ship are prepared by Chef Molnárka Péter.
Our Ship cruise starts around 19:00, and will anchor before the fireworks start (ships aren't allowed to sail during the show).
The cruising itself includes live music. The salon music is performed by three members of the Kodály Zoltán Awarded Hungária Folk Orchestra, including the world-famous violinist Vidák Zsigmond (awarded with the Bronze Merit Cross of the Hungarian Republic).
Detailed Program:
18:30 Meeting time at Jászai Mari tér,
19:00 cruise starts
20:55 the ship will anchor before the fireworks start (ships aren't allowed to sail during the show).
21:00 fireworks start
21:45 back to the pier (starting point)
Price of the Dinner & Cruise with live music + the watch of the fireworks from the Danube:
Cold entries
Spiced cottage cheese cream and traditional greaves cream
Alföld style goulash with small dumplings
Cold fruit soup
Warm main courses
Mini stuffed cabbage
Traditional chicken leg "Paprikasch"
Roasted chicken breast with basil-cheese sauce
Spicy pork rib with thyme – mustard sauce
Roasted sea fish with Chardonnay sauce
Garnishes and vegetarian
Grilled polenta with feta cheese
Homemade dumplings with spinach and mustard-
mushroom sauce
Grilled vegetables
Steamed jasmin rice with corn
Hash-brown potatoes
Steak potatoes
Fresh seasonal salads with dressings
Italian pasta salad
Caesar's salad
Sweet corn salad with mayonnaise
Home-made strudel
Somló style sponge cake
Dessert variations Európa style
Season fruit bask
Open bar!
Soft Open Bar
Unlimited drinks from the followings:
Dry Champagne, Sweet Champagne
Bárdosi Pinot Grigio 2014
Szekszárdi Civilis Cuvée 2013
Jandl Soproni Kékfrankos 2013
Juhász Kékfrankos Rosé 2013/14
Dreher Bak
Dreher alcoholfree
Dreher (draft beer)
Pilsner Urquell (draft beer)
Soft drinks
Pop drinks, Juices (Toma and Rauch products), Mineral water (Szentkirályi)
Warm drinks
Segafredo coffee variations
Dilmah tea variations
Open bar operates during the whole program!
Meeting point is at Jászai Mari Square
Address: Budapest, Jászai Mari tér


text:
More Crazy Stuff at the Valarium
Hank III's crew arrested, singer performs five-hour set
More crazy stuff went down at the Valarium last week when Hank III, son of Hank Williams Jr. and grandson of Hank Williams, played an epic five-hour set of country music, extending his Wednesday night concert well into Thursday morning in apparent protest after two members of his crew were arrested.
The July 15 show was billed as one set of country by Hank III and one set by Hank and his punk-metal band Assjack. Instead, concertgoers got about three sets' worth of Hank solo from about 10 p.m. to almost 3 a.m.
Hank III's manager and assistant manager were arrested for disorderly conduct at the site. The assistant manager was also charged with resisting arrest.
Valarium owner Gary Mitchell says he was out of town and doesn't know details of either the Hank III show or the 10 for $10 hardcore package tour that was canceled just minutes after starting when a large-scale brawl spilled into the parking lot.
"He just does what he wants to do," Mitchell says, downplaying the effect of the arrest on Hank III's performance. "There's no real rhyme or reason."
Seven people were arrested in the 10 for $10 incident.
Mitchell says Hank III has already promised to come back for another show soon. "He called Thursday and said he felt like he'd stiffed his hardcore fans," Mitchell says.
Local honky-tonkers J.C. and the Dirty Smokers, who were scheduled to play the after-party show at the adjacent Cider House, finally took the stage at 2 a.m. "Basically, I said, 'Since we're already set up and already have a stage, we might as well work on a couple of originals," says Dirty Smokers frontman J.C. Haun. "So we ended up having a rehearsal, basically."