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In This Ancient House (Momoshiki Ya)
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In This Ancient House (Momoshiki Ya) composed by Ruth Morris Gray. For SAB choir, Piano, Optional Finger Cymbals. Educational Octavo. Concert. Published by Heritage Music Press (LX.15-2407H).
This gentle setting of a traditional Japanese poem captures the mystery of ancient Japan, with its haunting melody and simple harmonies. The Japanese text alternating with the English translation is easy to learn and evokes images of ages past. Included are both a pronunciation and translation guide. The finger cymbals compliment the distinctly Asian flavor of this piece, featuring open fourths and fifths.
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Samsung Electronics said its third-quarter net profit nearly halved, as its mobile division continued to suffer from heightened global competition. Here's a look at five key takeaways from the company's difficult quarter. Read More »
Oct 30, 2014
Samsung Electronics said its third-quarter net profit nearly halved, as its mobile division continued to suffer from heightened global competition. Here's a look at five key takeaways from the company's difficult quarter. Read More »
Taiwan Semiconductor Manufacturing, which has boosted its profile in the chip-manufacturing industry by inking deals with Apple, has added LG Electronics to its list of customers for the high-tech chipsets used in smartphones.
LG Electronics said Friday it has developed its own microprocessor to power a variation of its flagship G3 smartphone – a first for the South Korean electronics giant. Read More »
As Apple's new large-screen iPhone starts to hit shelves around the world, the latest Samsung Electronics Galaxy Note 4 smartphone has also—quietly—begun presales. But the odds don't look great for the Note.
"Reviews on the new iPhone are just getting better and better, as more customers get their hands on them," said Lee Seung-woo, an analyst with IBK Securities in Seoul. Read More »
When LG Electronics released its latest flagship G3 phone in May, it clearly beat crosstown rival Samsung Electronics in one aspect: screen resolution.
The company's 5.5-inch phone came with what's called "Quad HD" resolution, equivalent of having 2560 x 1440 pixels or about four times a normal high-definition screen and nearly twice that of a full HD screen. The screens were developed by LG Display, which also makes displays for Apple's iPhones and iPads.
LG claims that its G3 phone was the first smartphone to use such a high-resolution screen. So far, the G3 phone has attracted positive reviews and among its rivals in South Korea, LG was the only mobile phone company to report upbeat earnings in the latest quarter. Read More »
Over the past week, investors, analysts, journalists and the like have all been focusing on Samsung's less-than-stellar performance from its smartphone business in the second quarter.
Yes, Samsung has been losing market share in smartphones in the global market and even in China, where Xiaomi overtook the company in terms of shipments in the second quarter to much surprise.
But the outlook is also looking murky for its other, lesser-known business – making the microprocessors that are widely used in Apple's iPhones and tablets. Samsung up until last year had a monopoly on Apple's supply but earlier this year, Taiwan Semiconductor Manufacturing began shipping them to Apple, according to people familiar with the matter. Read More »
What if you could see through your TV and roll it up in the future?
LG claims that it has developed a screen technology that would allow you to do so in the future. But just how long it might take for them to be available in the market is another question. Read More »
Samsung Electronics, which makes many of its own smartphone components, said that a small number of batteries used in its popular Galaxy S4 smartphones sold in Israel overheated and burned. Read More »
Samsung Electronics said five of its Galaxy-branded smartphones and tablets that come with its enterprise security software recently received approval from the U.S. Defense Information Systems Agency, allowing them to be listed as an option for officials. Read More »
When it comes to tablet sales, Samsung Electronics Co. may be its own worst enemy.
The Suwon, South Korea-based company is busy gearing up for its next major product launch–a splashy event to introduce a new line of tablets, slated to take place in two weeks at New York's historic Madison Square Garden. Read More »
Samsung Electronics Co. on Tuesday reported a modest decline in operating profit and a small rebound in net profit, and said its new flagship Galaxy S5 smartphone was off to a strong start.
The results were roughly in line with guidance and expectations. Nevertheless, investors Tuesday sent Samsung's shares to their biggest one-day decline in a month, pushing them down 2% to a four-week low, on a day when Seoul's broader Kospi Composite slipped 0.2%.
On Wednesday, the shares fell a further 1.3%, bringing the decline in the past week to 4.5%.
Why the recent decline? Read More »
Korea Real Time provides sharp analysis and insight into what's making news on the Korean peninsula. We chronicle the growing pains of South Korea — a country that has skyrocketed into the club of the world's richest nations but now faces significant headwinds, and shine a spotlight on one of the world's biggest geopolitical flashpoints: North Korea. Drawing on the expertise of The Wall Street Journal and Dow Jones Newswires, we'll tell the stories behind the headlines in business, economics, politics, culture and lifestyle. You can contact the editors at firstname.lastname@example.com

subset: commoncrawl


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rock face edge or flat polish on Lido granite
rjdaySeptember 24, 2012
We are remodeling our 100 yr old lake cottage. Cabinets are a distressed Alder wood. We are using Lido granite on kitchen counters & Natueno Gold on island. Considering a rock face edge on both. Any comments?
Is that the chiseled look? If so, I'm sorry to say I usually only like those outdoors. But, that is not to say in a lake cottage with the distressed alder wood it won't look great.


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REGION: Veterans Day events planned around county
Weekend celebration of veterans planned
MENIFEE ---- The city will hold a weekend Veterans Day celebration Saturday and Sunday.
The weekend will kick off with the second annual Veterans Day Memorial 5K run, a chip-timed race beginning at 8 a.m. Saturday in Wheatfield Park and traveling up and over Bell Mountain. Military personnel will be in attendance and military equipment will be on display at the park. Participants will receive a T-shirt and commemorative dog tag. Proceeds will benefit the veterans memorial at the park. Registration is available online at active.com.
A Veterans Day ceremony will be featured at 10 a.m. Sunday at Wheatfield Park. The free event, developed in partnership with the city's Veterans Memorial Committee, will honor and celebrate all veterans and include a flyover arranged with March Air Reserve Base.
Families may honor veterans and military personnel currently serving through the city's Military Banner Program. Banners, which may include a photo, are hung from city light poles on Menifee streets. The cost is $100 and includes installation.
Wheatfield Park is at 30627 Menifee Road.
For information, call (951) 672-6777.
Veterans Day Parade scheduled for Sunday
MURRIETA ---- The 10th annual Veterans Day parade will begin at 1 p.m. Sunday in downtown Murrieta.
The parade will begin on Ivy Street, travel north on Washington Avenue, then turn right on B Street before concluding in Town Square Park.
After a military flyover, 60 entries are expected to participate, including military and veterans groups, Scouts, dance teams and equestrian units. Also participating will be a color guard and tanks from Camp Pendleton.
With the parade on a Sunday, the start was pushed back from its usual morning timeframe to 1 p.m.
For information, call (951) 304-2489.
World War II POW to speak at event
RIVERSIDE ---- Former World War II prisoner of war Cecil Davis of San Jacinto will be the keynote speaker at Sunday's 34th Riverside National Cemetery Veterans Day ceremony.
Shot down in the B-17 he was piloting, Davis was freed when Allied forces liberated the Dachau prison camp, where he was working as a prison laborer.
Sunday's program will begin at 11 a.m. in keeping with the tradition that began when the Armistice was signed at the 11th hour of the 11th day of the 11th month, ending World War I.
The Riverside Concert Band will perform patriotic music beginning at 10:30 a.m. The program will include flyovers of current and vintage military aircraft.
The Order of Daedalians, Thirtieth Flight will observe its annual Veterans Day service at the cemetery's flag pole plaza at the same time.
Veterans Day marks the anniversary of the cemetery's opening in 1978. Nearly 215,000 veterans and their family members have been interred at Riverside National Cemetery, the third-largest of the 131 national cemeteries.
The cemetery is at 22495 Van Buren Blvd. in Riverside.
For information, call (909) 957-3982.
Picnic, concert to honor veterans
TEMECULA ---- The Community Recreation Center amphitheater will play host to a picnic and concert to honor veterans Sunday.


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Page 1
Functional coupling of angiotensin II type 1
receptor with insulin resistance of energy substrate
uptakes in immortalized cardiomyocytes (HL-1 cells)
C Alfarano1, L Sartiani2, C Nediani2,3, E Mannucci4, A Mugelli1,2, E Cerbai1,2and L Raimondi1
1Department of Preclinical and Clinical Pharmacology, University of Florence, Florence, Italy;2Center of Molecular Medicine
(C.I.M.M.B.A.), Department of Preclinical and Clinical Pharmacology, University of Florence, Florence, Italy;3Department of
Biochemical Sciences, University of Florence, Florence, Italy and4Department of Critical Care Medicine and Surgery, Unit of
Gerontology and Geriatrics, University of Florence and Azienda Ospedaliera Careggi, Florence, Italy
Background and purpose: Increased angiotensin II levels and insulin resistance coexist at the early stages of
cardiomyopathies. To determine whether angiotensin II increases insulin resistance in cardiomyocytes, we studied the effect
of angiotensin II on basal and insulin-stimulated transport rate of energy substrates in immortalized cardiomyocytes (HL-1
Experimental approach: Glucose and palmitic acid uptakes were measured using [3H]2-deoxy-D-glucose and [14C]palmitic
acid, respectively, in cells exposed or not exposed to angiotensin II (100nM), angiotensin II plus irbesartan or PD123319, type
1 and 2 receptor antagonists, or PD98059, an inhibitor of ERK1/2 activation. Cell viability, DNA, protein synthesis and surface
area were evaluated by the MTT test, [3H]thymydine, [3H]leucine and morphometric analysis, respectively. Type 1 receptor
levels were measured by western blot analysis.
Key results: Basal uptakes of glucose and palmitic acid by HL-1 cells (0.37±0.07 and 7.31±0.22pmol per 104cells per min,
respectively) were both stimulated by 100nM insulin (þ91 and þ64%, respectively). Cells exposed to angiotensin II remained
viable and did not show signs of hypertrophy. In these conditions, the basal palmitic acid uptake of the cells increased
(11.41±0.46pmol per 104cells per min) and insulin failed to stimulate the uptake of glucose and fatty acids. Changes in the
rate of uptake of energy substrates were prevented or significantly reduced by irbesartan or PD98059.
Conclusions and implications: Angiotensin II is a candidate for increasing insulin resistance in cardiomyocytes. Our results
suggest a further mechanism for the cardiovascular protection offered by the angiotensin II type 1 receptor blockers.
British Journal of Pharmacology (2008) 153, 907–914; doi:10.1038/sj.bjp.0707563; published online 5 November 2007
Keywords: HL-1 cells; glucose uptake; fatty acid uptake; angiotensin II type 1 receptor blockers; insulin resistance; hypertrophy
Abbreviations: AT1, angiotensin II type 1 receptor; AT2, angiotensin II type 2 receptor; CPM, counts per minute; ERK1/2,
extracellular signal-regulated kinase; FAT/CD36, fatty acid transporter, insulin-sensitive; GAPDH, glyceralde-
hyde-3-phosphate dehydrogenase; GLUT1, type 1 glucose transporter; GLUT4, type 4 glucose transporter; HL-
1 cells, immortalized cardiomyocytes
There is increasing evidence that alterations in energy
substrate transport and utilization by cardiac myocytes
represent a primary cause of the pathogenesis of heart
diseases including diabetic cardiomyopathy (Fang et al.,
Physiologically, about 80% of the energy required by a
healthy adult heart is supplied by the intracellular oxidation
of fatty acids, whereas the remaining 20% depends on
glucose use. The relative percentage of each of these fuelling
substrates is finely regulated by hormone levels in the
microenvironment and this includes the concentration of
insulin. In fact, insulin not only helps to maintain the
correct myocardial energy supply by increasing types 4 and 1
glucose transporter (GLUT4 and GLUT1) activities (Opie,
2004), but also controls the intracellular availability of fatty
acids. Recent evidence demonstrates that insulin regulates
the docking towards plasma membrane of a translocase (the
FAT/CD36 (fatty acid transporter, insulin-sensitive)) that
works in addition to simple diffusion and to other carrier-
mediated transports (Luiken et al., 2002a,b). While the
Received 16 July 2007; revised 20 September 2007; accepted 3 October 2007;
published online 5 November 2007
Correspondence: Professor L Raimondi, Department of Preclinical and Clinical
Pharmacology, University of Florence, Viale G Pieraccini, 6, Florence 50129,
Italy, Italy.
E-mail: email@example.com
British Journal of Pharmacology (2008) 153, 907–914
& 2008 Nature Publishing Group All rights reserved 0007–1188/08 $30.00
Page 2
signalling cascade involving the inositol triphosphate kinase
pathway has been recognized as part of the insulin-regulated
GLUT4 and FAT/CD36 trafficking, less is known about
the subsequent common and/or distinct signalling steps
involved (Luiken et al., 2004).
In the heart of insulin-resistant animals, the relative
percentage of available intracellular glucose and fatty acids
changes. In particular, the FAT/CD36 stabilizes at the plasma
membrane and a lower amount of GLUT4 molecules is able
to move towards plasmalemma (Bonen et al., 2002; Coort
et al., 2004) resulting in an increased intracellular availability
of fatty acids. While this condition from one side may
saturate the mitochondrial b-oxidation, enhancing tissue
fatty acid storage (Stanley et al., 1997), it also can further
reduce the glucose entering the myocardial cells. On the
whole, this vicious cycle exacerbates insulin resistance
further by reducing the glucose and lactate uptake and
The effects of angiotensin II on the insulin sensitivity of
glucose uptake are not consistent and depend on cell type
(Izawa et al., 2005; Juan et al., 2005). Also, its direct effect on
the basal and insulin-stimulated glucose and fatty acid
transport rate has not been elucidated in single cardio-
myocytes. However, angiotensin II type 1 receptor (AT1)
blockers are widely used, clinically; they represent a first-line
approach in reducing the cardiovascular risk in diabetic
patients (Schmieder, 2005), but their role in ameliorating
insulin resistance is not proved (Lerch et al., 1998). These
drugs have consistently been reported to be neutral with
regard to insulin sensitivity (Lerch et al., 1998), but have
proven effectiveness in preventing diabetic electrophysiolo-
gical remodelling, probably by counteracting the dysregula-
tion of energy substrate supplementation of cardiomyocytes
(Raimondi et al., 2004).
HL-1 cells are an immortalized cardiac cell line that retain
a differentiated morphology (Sartiani et al., 2002; White
et al., 2004; Fukuda et al., 2005; Clarke et al., 2006) and have
been used previously to study hormone-dependent glucose
and fatty acid metabolism (Palanivel et al., 2006). Moreover,
HL-1 cells express on their surface several hormone receptors
including the AT1receptor (Filipeanu et al., 2004). For all
these reasons, HL-1 cells represent an excellent model for
studying the effects of angiotensin II on cardiomyocyte
We measured the basal and insulin-stimulated glucose and
fatty acid uptake in HL-1 cells cultured in the absence or in
the presence of angiotensin II, a condition mimicking a
pathological microenvironment.
HL-1 cells were cultured as described previously (Sartiani
et al., 2002). Briefly, cells were grown as a monolayer (371C,
5% CO2) in culture flasks, dishes and plates precoated with
2mgcm?2fibronectin dissolved in a 0.02% gelatin solution.
HL-1 cells were maintained in Claycomb medium supple-
mented with 10% foetal bovine serum, 4mM L-glutamine,
L-ascorbic acid 30mM) and 1?
solution (standard medium). The medium was changed
every 24–48h.
To mimic a pathological microenvironment, HL-1 cells
were cultured in standard medium up to 90% of confluence
and then shifted to a standard medium with low serum
(0.1% serum), in the absence of noradrenaline, but with the
addition of angiotensin II (100nM). Cell exposure to
angiotensin II was stopped after 18h of culturing at 371C
in 5% CO2. Where stated, angiotensin II exposure was
carried out in the presence of either an AT1(irbesartan; 1mM)
(PD123319; 1mM) or an inhibitor of extracellular signal-
regulated kinase (ERK)1/2 activation (PD98059; 10mM).
receptor (AT2)antagonist
Glucose and fatty acid uptake in HL-1 cells
The basal and insulin-stimulated glucose and long-chain
fatty acid transports were measured radiochemically in HL-1
cells seeded in 96-multiwell plates and cultured up to 90% of
confluence (1.8±0.4?104cells). In some plates, angiotensin
II was added as described above; other plates were cultured
for the same time in Claycomb medium (containing 0.1%
serum) and referred to as 'control'. At the end of the
incubation, plates were thoroughly washed with saline
For glucose uptake experiments, cells were diluted with
glucose-free Krebs phosphate buffer (pH 7.8; Raimondi et al.,
2004), whereas for palmitic acid uptake, cells were incubated
in the same buffer containing 5mM glucose and ranolazine
(1mM), an inhibitor of fatty acid oxidation (Stanley, 2005).
The effect of insulin on energy substrate uptake was
evaluated by exposing cells to the hormone (humulin) from
Eli Lilly (Toronto, Canada) for 30min before adding [3H]2-
deoxy-D-glucose (10mM; 1mCi per well) or a [14C]palmitate/
BSA complex (1mCi per well; molar ratio 0.3; final concen-
tration 100mM) (Chabowski et al., 2005). The uptake of
glucose and palmitic acid was measured 10 and 5min,
respectively, after the addition of labelled substrates. Cells
were then extensively washed with cold Krebs buffer, and the
radioactivity incorporated was measured by scintillation
counting (Raimondi et al. 2004).
Non-transporter-dependent glucose and palmitic acid
uptake were determined in cells pretreated for 30min with
phloretin (10mM) before the addition of labelled substrates.
The residual (phloretin-insensitive) radioactivity was sub-
tracted from each measurement obtained. The involvement
of inositol triphosphate kinase activation in both glucose
and fatty acid uptake was evaluated by pretreating the cells
for 30min with wortmannin (100nM) before the addition of
Each pharmacological intervention (angiotensin receptor
antagonists and ERK1/2 inhibitor) was tested for its ability to
modify glucose and fatty acid uptake. As none of the drugs
used affected the basal uptake of either glucose or fatty acid,
the results obtained from the cells exposed to each
pharmacological treatment were pooled with the basal
values obtained in control cells. Results are presented as
pmol per 104cells per min for glucose and fatty acid uptake
or as arbitrary units (where the effect of each stimulation is
compared to the respective basal uptake which is taken as
Angiotensin II and HL-1 cells energy supply
C Alfarano et al
British Journal of Pharmacology (2008) 153 907–914
Page 3
100). The values shown represent the means±s.e.mean of
5–18 different experiments, each run in triplicate.
HL-1 viability, hypertrophy and cell surface
Viability, protein and DNA synthesis were evaluated in sub-
confluent HL-1 cells, 1.7±0.8?105cells cultured in six
multiwell plates, that had or had not been exposed to
angiotensin II. Cells were then washed with 0.1 M phosphate
buffer pH 7.8 containing 0.1 M NaCl (phosphate-buffered
saline) before the addition of phosphate-buffered saline
containing 0.5mgml?1
formazan production after 2h was evaluated colorimetrically
at 570nm. Results are expressed as the mean±s.e.mean of
the OD recovered from three experiments, each run in
(Mosmann, 1983).The
DNA and new protein synthesis
Cells were plated as above and then exposed to angiotensin
II. At the beginning of the exposure, cells were labelled with
[3H]thymidine or [3H]leucine (0.5mCi per well). After 18h,
the radioactive medium was discarded, cells were washed
three times with ice-cold phosphate-buffered saline and
incubated with 5% trichloroacetic acid (TCA) on ice for
30min and solubilized in 0.5N NaOH. After the sample had
been neutralized with 0.5N HCl, the radioactivity incorpo-
rated was counted in a scintillation counter (Packard
Instruments, Minneapolis, MN, USA). Results are shown as
the counts per minute (CPM) per well, and they represent
the mean±s.e.mean of three experiments, each run in
triplicate. Cells deprived of serum for 24h before the
addition of [3H]thymidine or [3H]leucine did not incorporate
significantly different amounts of radioactivity compared to
those with normal serum (data not shown).
For these measurements, cells cultured in 75cm2flasks and
exposed to angiotensin II as described above were used.
Briefly, control and exposed cells were stained with haema-
toxylin/eosin, and four randomly chosen microscopic fields
per flask were used for analysis. The microscopic fields were
registered by a closed-circuit television camera (WPI, Sarasota,
FL, USA) applied to a Reichert-Jung Microstar IV light
microscope (Cambridge Instruments, Buffalo, NY, USA) and
interfaced with a personal computer through a Matrox Marvel
G400-TV digitizing card (Matrox Graphics, Dorval, QC,
Canada). On the digitized images, cell outlines were traced
and the surface area was calculated using the Scion Image Beta
4.0.2 image analysis programme (Scion Corp., Frederick, MD,
USA) thresholding on blank, cell-free aerial spaces. The mean
values (±s.e.mean) of cell areas were then calculated for each
experimental group. From 80 to 120 cells were measured in
each randomly selected field (Bani et al., 2006).
Expression of angiotensin II type 1 receptor
Protein lysates from 75cm2flasks of HL-1 cells (90–95%
confluent) not exposed or exposed to angiotensin II were
prepared. Briefly, after the exposure medium had been
removed and the cells extensively washed with ice-cold
phosphate-buffered saline, the cells were scraped off the
flasks with lysis buffer of the composition (in mM) Tris-HCl
(50) (pH 7.5), EDTA (1), NaCl (150), complete protease
inhibitor cocktail tablet, sodium orthovanadate (1) and NaF
(10) and then homogenized. The suspension was centrifuged
(1000g for 10min at 41C) to remove cell debris. The
resulting supernatant was frozen at –801C for later analysis
by immunoblotting. The protein concentration of the crude
lysate was determined by the BCA protein assay reagent kit
from Pierce (Rockford, IL, USA).
Protein samples were subjected to 4–12% (w/v) acrylamide
gel and transferred to polyvinylidene difluoride membranes.
The membrane was probed with the primary antibody
(1:1000 dilution) against AT1or glyceraldehyde-3-phosphate
dehydrogenase (GAPDH; 1:1000 dilution) overnight at 41C.
Antibody binding was detected with a goat-anti-rabbit
horseradish peroxidase (1:10000 dilution) secondary anti-
body. Detection of the immunocomplex was carried out by
chemiluminescence. GAPDH expression was used as a
'housekeeping protein' and to evaluate transfer efficiency
(Rajapurohitam et al., 2006).
Data analysis
Data are expressed as mean±s.e.mean. Results were analysed
using Student's unpaired t-test with Welch's correction or
with one-way ANOVA (Dunnett's test). A P-valueo0.05 was
considered to be significant. Calculations were made using
GraphPad Prism and Instat version 4.0 for Windows
(GraphPad Software, San Diego, CA, USA).
HL-1 cells were obtained from Dr W Claycomb (Louisiana
State University Medical Center, New Orleans, LA, USA).
Fibronectin, 0.02% gelatin solution, noradrenaline, ranolazine,
phloretin, wortmannin, insulin, 3-[4,5-dimethylthiazol-2yl]-2,
5-diphenyltetrazolium bromide, complete protease inhibitor
cocktail tablet, sodium orthovanadate and goat-anti-rabbit
horseradish peroxidase were obtained from Sigma (St Louis,
MO, USA); Claycomb medium and foetal bovine serum
from JRH Biosciences (Andover, UK); humulin from Eli
[3H]thymidine and [3H]leucine from Amersham Life Science
(Little Chalfont, UK); BCA protein assay reagent kit from
Pierce; acrylamide gel (Nu-Page Gel) from Invitrogen
(Milan, Italy); GAPDH from St Cruz Biotechnology Inc.
(St Cruz, CA, USA).
HL-1 cardiomyocytes present insulin-sensitive glucose and
palmitic acid uptakes
As described previously (Chaudary et al., 2002; Palanivel
et al., 2006), phloretine-sensitive mechanisms govern the
basal supply of glucose and long-chain fatty acids, measured
Angiotensin II and HL-1 cells energy supply
C Alfarano et al
British Journal of Pharmacology (2008) 153 907–914
Page 4
as palmitate uptake, in HL-1 cardiomyocytes in our experi-
mental conditions. In particular, the palmitate uptake
accounted for about 95% and the glucose for 5% of the
total energy substrate available (Table 1).
The rate of the two uptakes increased, in a concentration-
dependent manner, following acute exposure of cells to
insulin. As shown in Figure 1a, insulin increased, in a
concentration-dependent manner, the transport of glucose
and of palmitate. Similar values of potency were obtained
(EC50 values being 7.17±1.71nM, (confidence limit) CL:
2.57–14.14; and 4.65±1.51nM, CL: 1.42–15.22 for glucose
and palmitate, respectively) and maximum effect (þ91%
and þ64% for glucose and palmitate, respectively) was seen
with 100nM insulin (Figure 1b). Pre-incubating the cells with
wortmannin significantly (Po0.05 vs insulin effect; n¼6)
reduced the increased uptake of glucose and palmitate
induced by insulin (Figure 1b). This suggests that inositol
triphosphate kinase is involved in the intracellular signalling
regulating the docking towards plasmalemma of both
Effects of long-standing exposure to angiotensin II
Cell viability. Exposing cells to angiotensin II (100nM) for
18h did not affect cell viability; indeed, similar values of
oxidized formazan were recovered in control and in
angiotensin II-exposedcells
0.58±0.02, respectively, n¼3 different cell passages, each
determination run in quadruplicate).
(OD: 0.55±0.07 and
The basal transport rate of glucose and palmitate.
angiotensin II exposure for 18h did not change the basal
uptake of glucose, it maximally increased cell palmitate
uptake rate. In fact, as shown in Table 1, the palmitate
uptake of exposed cells achieved the same rate as that
induced by 100nM insulin in control cells (see above results).
Insulin stimulation of energy substrate available.
cells, acute administration of insulin failed to stimulate the
uptake of either glucose or palmitate (Figures 2 and 3). In
In exposed
fact, the dose that induced maximum stimulation (100nM
insulin) in control cells produced a glucose uptake of
0.44±0.05pmol per 104cells per min (þ20% of basal;
Figure 2) and a fatty acid uptake of 12.50±0.47pmol per 104
cells per min (þ13% of cell uptake in the absence of insulin).
Angiotensin II type 1 receptor expression.
of the AT1receptor did not change in cells exposed for 18h
to angiotensin II (Figure 4a).
The expression level
Table 1
challenged with different treatments
Basal glucose and palmitic acid uptake rate in HL-1 cells
TreatmentsGlucose uptake (pmol
per104cells per min)
Palmitic acid uptake (pmol
per104cells per min)
Control (n¼18)
Angiotensin II
Angiotensin IIþIRB
Abbreviation: IRB, irbesartan.
**Po0.01, *Po0.05 vs cells not exposed.
The basal glucose and palmitic acid uptake rate was measured in HL-1 cells not
exposed and exposed to angiotensin II as described in Methods.
Figure 1
(immortalized cardiomyocytes) HL-1 cells. (a) Glucose and palmitate
uptakes were measured radiochemically as described in Methods.
Insulin stimulates in a concentration-dependent manner the rate of
both transports. Insulin potency (EC50) was calculated by the fitting
of experimental points. (b) Pre-incubation of cells with wortmannin
reduced the insulin stimulation of glucose and palmitic acid uptake.
Results are presented as stimulated rate compared to the basal
transport rate, taken as 100, and they represent the mean±s.e.mean
of at least eight (a) or six (b) experiments run in triplicate. For the
basal uptake values see Table 1. *Po0.05 vs insulin effect in the
absence of wortmannin.
The insulin-stimulated glucose and palmitate transport in
Angiotensin II and HL-1 cells energy supply
C Alfarano et al
British Journal of Pharmacology (2008) 153 907–914
Page 5
Cell hypertrophy.
protein content, the cell surface area, the DNA and protein
synthesis occurring during angiotensin II exposure were
Our results show that exposure to angiotensin II did not
modify either the total cell protein content (0.34±0.15 vs
As an index of hypertrophy, the total cell
0.28±0.08mgml?1in control cells), the 18h related DNA
and protein synthesis (Figure 4b) or the cell surface area
(Figure 4c). Altogether these findings suggest that angio-
tensin II does not induce hypertrophy in these cells.
The effect of blocking angiotensin II type 1 receptors on insulin
resistance of the energy substrate uptake
As AT1 receptors are clearly present in our cells, we
investigated the effect of blocking these receptors on
the insulin resistance elicited by angiotensin II exposure.
Irbesartan (1mM), an AT1antagonist, or PD98059 (10mM), an
inhibitor of ERK1/2 activation, were added during the
exposure of the cells to angiotensin II. In addition, since
the presence of AT2 receptors could not be excluded,
experiments using an AT2 receptor antagonist were also
run for comparison.
The effect of irbesartan and ERK1/2 inhibition on the basal and
insulin-stimulated glucose and palmitate uptake.
of irbesartan and PD 98059 prevented most of the changes in
energy substrate uptake induced by angiotensin II. In fact,
under these conditions, cell palmitate uptake rate did not
increase (Table 1) and, more importantly, cells regained some
responsiveness to insulin. In fact, 100nM insulin stimulated
further (þ41%) cell palmitate uptake; in terms of pmol, this
represents 70% of the maximum insulin effect measured in
control cells (Figure 3a).
As regard to glucose uptake, in the presence of irbesartan,
the uptake induced by insulin was 0.58±0.08pmol per 104
cells per min (þ77% of basal), a value not significantly
different from that induce by insulin in control cells
(0.70±0.11pmol per 104cells per min; þ90% of basal;
Figure 2).
Similar results were obtained in cells exposed to PD98059.
As with irbesartan, inhibition of ERK1/2 activation pre-
vented the angiotensin II-dependent increase of cell palmitic
acid uptake (Table 1). This allowed insulin to fuel the uptake
further þ37% (Figure 3b). As with irbesartan, in terms of
pmol produced, this stimulation represented 69.7% of those
produced by insulin in control cells (Figure 3a).
Again, the incubation with angiotensin II in the presence
of PD98059 restored the maximum insulin stimulation on
the glucose uptake (0.65±0.11pmol per 104cells per min;
Figure 2b).
Conversely, in cells exposed to angiotensin II and
PD123319, palmitic uptake remained high (see Table 1),
and the effect of insulin on the uptake of both energy
substrates uptakes was attenuated (Figures 2 and 3).
The presence
Our results demonstrate that an 18h exposure to angioten-
sin II has the potential to hamper the supply of energy
substrates of HL-1 cardiomyocytes. In particular, angiotensin
II exposure increased cell palmitate uptake rate and reduced
the insulin-stimulating activity of insulin (insulin resistance)
on the uptake of both glucose and palmitate. Furthermore,
angiotensin II-related insulin resistance of substrate uptakes
Figure 2
insulin resistance of glucose uptake. (a) Concentration-dependent
effect of insulin (from 5 to 300nM) on glucose transport in cells
exposed to angiotensin II, angiotensin II plus irbesartan (IRB, 1mM) or
PD98059 (10mM) or angiotensin II plus PD123319 (1mM). Results are
the mean±s.e.mean of 8–18 experiments run in triplicate and are
presented as stimulation of their basal uptake rate (taken as 100).
Lines represent fitting of data points. (b) The maximum value of
insulin (100nM)-stimulated uptake (as calculated by fitting curves
from (a) and from Figure 1) in HL-1 cells challenged with different
compounds. Each column is the mean±s.e.mean of 5–18 experi-
ments run in triplicate. **Po0.01, compared to insulin maximum
effect in control cells.
Pharmacological modulation of angiotensin II-induced
Angiotensin II and HL-1 cells energy supply
C Alfarano et al
British Journal of Pharmacology (2008) 153 907–914
Page 6
appeared to involve different mechanisms and occurred
independently of cell hypertrophy. In our experimental
conditions, in contrast to that observed in neonatal
cardiomyocytes (Rajapurohitam et al., 2006), angiotensin II
did not evoke any change either in the cell surface area or in
DNA and protein synthesis. Taken together, these results
suggest that the onset of this metabolic re-arrangement is an
early indication of a predisposition to cardiomyopathies.
Our results confirm that HL-1 cells possess, in addition to
glucose transport systems (Chaudary et al., 2002), a phloretin-
sensitive mechanism involved in the intracellular transport
of long-chain fatty acids. Both transporters respond similarly
to insulin stimulation; insulin increased the rate of uptake of
glucose and palmitate in a wortmannin-sensitive manner.
While these results clearly indicate the involvement of
GLUT4 and GLUT1 in the transport of glucose, they do not
allow us to draw conclusions regarding the nature of
the fatty acid carrier (Fischer et al., 1997). However, since
FAT/CD36 is, so far, the only insulin-sensitive fatty acid
carrier known (Chabowski et al., 2005), it is likely that it is
involved in our experimental model.
Our data allow us to hypothesize that angiotensin II has
different effects on FAT/CD36 and GLUT1/GLUT4 recruit-
ment and, because of this, the insulin resistance induced by
angiotensin II involves different mechanisms. In fact, cells
exposed to angiotensin II showed the same GLUT1 activity
as those not exposed, whereas the uptake of fatty acid by the
exposed cells was increased maximally. This indicates that
angiotensin II has 'insulin-like' effects at FATCD36, stimulat-
ing its trafficking maximally and additionally stabilizing the
transporters at the plasma membrane (Coort et al., 2004). As
a consequence of this, insulin cannot further stimulate FAT/
CD36 in cells that have been in contact with angiotensin II,
even when angiotensin II is not present in cell medium. The
reduction of insulin function resulted from changes in FAT/
CD36 homeostasis occurring during the 18h of exposure to
angiotensin II. In addition, since cell surface area and protein
synthesis did not change following angiotensin II, altera-
tions in the sarcolemmic density of the transporters is
unlikely to play a major role. However, whatever the
mechanism is (saturation, desensitization for overactiva-
tion), a previous exposure to angiotensin II reduced the
susceptibility of the fatty acid transporters to the effects of
In contrast, insulin resistance of glucose uptake occurred
in the absence of any increase in the basal transport rate of
this sugar. In most cells, the ubiquitous GLUT1 mainly
accounts for the basal transport rate, but this transporter is
much less responsive to insulin stimulation than GLUT4
(Fischer et al., 1997). Thus, the finding that angiotensin II
exposure did not affect the basal transport of glucose
(GLUT1) suggests that this hormone interferes preferentially
with the insulin receptor cascade controlling GLUT4 recruit-
ment in insulin-sensitive cells. A lack of an effect on GLUT1
rate is in line with the absence of hypertrophy in our cell
model. Hypertrophic cardiomyocytes have been shown to
exhibit a clear-cut increase in glucose consumption and
GLUT1 activity (Montessuit and Thorburn, 1999).
If angiotensin II promotes cardiomyocyte insulin resis-
tance, recovery of insulin sensitivity may be induced by
Figure 3
insulin (100nM)-stimulated uptake (pmol per 104cells per min) in HL-1 cells challenged with different compounds is presented. Each column is
the mean±s.e.mean of 5–18 experiments run in triplicate. **Po0.01 and *Po0.05 compared to uptake in control cells, and
compared to insulin effect in control cells. (b) Concentration-dependent stimulation of palmitic acid transport induced by insulin (from 5 to
300nM) was evaluated radiochemically, as described in Methods, in cells exposed to angiotensin II, angiotensin II plus irbesartan (IRB, 1mM) or
PD98059 (10mM) or angiotensin II plus PD123319 (1mM). Results are the mean±s.e.mean of 5–18 experiments run in triplicate and are
presented as arbitrary units (see text for details). Lines represent fitting of data points.
Pharmacological modulation of angiotensin II-induced insulin resistance of palmitate uptake. (a) The maximum absolute value of
Angiotensin II and HL-1 cells energy supply
C Alfarano et al
British Journal of Pharmacology (2008) 153 907–914
Page 7
drugs interfering with the production or effects of angio-
tensin II. Our results suggest that this is the case. The insulin
resistance of glucose uptake caused by angiotensin II was
removed or significantly reduced by inhibiting the AT1
cascade. Alterations due to angiotensin II exposure were
similarly reversed by blocking AT1receptors with irbesartan
or by inhibiting ERK1/2 activation, a downstream effector of
the receptor cascade (Izawa et al., 2005). Moreover, irbesartan
and PD98059 prevented the angiotensin II stimulation of
cell fatty acid uptake confirming that this effect is under the
control of AT1. However, in contrast to glucose uptake, the
reduction of insulin stimulation of fatty acid uptake was not
completely attenuated by these drugs but significantly
reduced. The reason for this difference is unknown at the
present and different hypotheses have been proposed, such
as inappropiate irbesartan concentration, angiotensin II
receptor-independent effects, type 2 receptor effects un-
masked by AT1blockade or different pools of FATCD36 in
cell populations, alteration of the cycling–recycling rate of
FAT/CD36 at the plasma membrane. Moreover, while the
involvement of ERK1/2 in reducing insulin-dependent
glucose uptake has been described previously in vascular
cells (Izawa et al., 2005), this is the first time that this kinase
has been shown to play a role in the docking of both glucose
and palmitic acid transporters in cardiomyocytes. This
suggests that similar intracellular mechanisms govern the
cycling of GLUT4 and FAT/CD36 and further supports the
hypothesis that they coexist in the same vesicles (Luiken
et al., 2002a).
On the whole, prolonged exposure to angiotensin II causes
metabolic responses in HL-1 cells that are largely—if not
solely—dependent on AT1 receptors. On the basis of the
present results, it is unlikely that AT2receptors are involved
in the control of insulin-mediated modulation of substrate
In conclusion, our data demonstrate that, in addition to
hyperglycemia (Fang et al., 2004), angiotensin II may be key
factor in the onset of cardiac insulin resistance, an early
metabolic defect leading to the occurrence of metabolic
adaptations in the myocardium that progressively worsen its
performance (Chen et al., 1984).
Angiotensin II, by hampering insulin-regulated fatty acid
(that is, FAT/CD36) and glucose transport, is a probable
candidate for modifying the insulin response of energy
substrates in cardiomyocytes. Quite obviously, myocardial
insulin-induced glucose disposal can hardly be of relevance
for carbohydrate metabolism in the whole body; however,
the onset of myocardial insulin resistance may play a crucial
role in the development of cardiomyopathies.
Our observations in HL-1 cardiomyocytes have all the
limitations of an in vitro study, but our results identify a
direct role of AT1blockers in removing or ameliorating the
angiotensin II-dependent dysregulation of energy substrate
supply. The finding that irbesartan did not exert any effect
per se (that is, in the absence of angiotensin II), strongly
indicates that it opposes the adverse metabolic effects
elicited by angiotensin II by blocking AT1receptors. Hence,
these findings support a local effect of angiotensin II and
indicate an additional mechanism involved in the cardio-
vascular protection offered by AT1blockers
(GGP05093). We thank Bristol Meyer Squibb for providing
workwas supportedbygrants fromTelethon
Conflict of interest
The authors state no conflict of interest.
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text:
James Loney 1B TB 9 Days
Loney has gone 6-of-21 with two doubles so far through eight spring games and does not seem to have any threats to his potential playing time heading into 2015.
Loney has produced a solid .294/.342/.404 slash over the past two seasons as the Rays' regular first baseman, playing in 158 and 155 games respectively. The nine-year veteran appears to be on track to do the same in 2015, as he heads into the second year of a three-year, $21 million contract.
James Loney 1B TB 6 Months
Loney is not in the lineup Wednesday against the Red Sox, Roger Mooney of the Tampa Tribune reports.
Loney will get a rest as Sean Rodriguez fills in at first in his place. He had started seven games in a row before Wednesday, adding eight hits in that time.
James Loney 1B TB 6 Months
Loney is not in the lineup for Sunday's game against the Blue Jays.
Loney will get a day off as the Rays go with a right-heavy lineup against Blue Jays starter Mark Buehrle. Sean Rodriguez will get the start at first base in Loney's place.
James Loney 1B TB 7 Months
Loney went 4-for-6 with a solo homer and one run scored in Sunday's 7-5 loss to the Orioles.
After scuffling through a 3-for-21 skid over his previous six games, Loney broke out for his first four-hit effort of the season Sunday afternoon. The 30-year-old first baseman has been a consistent contributor here in 2014 for the Rays, as he leads the team in both hits (154) and batting average (.286).
James Loney 1B TB 7 Months
Loney is out of the lineup Thursday against the Blue Jays, Marc Topkin of the Tampa Bay Times reports.
Loney will be out of the lineup for the first time since Aug. 23, after starting the previous 11 games at first base for the Rays. It's hard to argue with the decision, since Loney is batting just 6-for-24 (.250) over his career against Blue Jays lefty Mark Buehrle, who will take the hill Thursday. Sean Rodriguez will step into the lineup in Loney's stead.
James Loney 1B TB 7 Months
Loney went 1-for-4 with a double, one RBI and a run scored in Saturday's 7-0 win over the Red Sox.
Loney has now gone 7-for-19 during a modest five game hitting streak, as the 30-year-old first baseman continues to swing one of the most consistent bats in the Rays' lineup this season.
James Loney 1B TB 7 Months
Loney is not in the lineup Thursday against Detroit, the Tampa Bay Times reports.
Loney has started every game since August 9 and will receive the day off with lefty David Price on the hill for Detroit. Sean Rodriguez will bat sixth and get the start at first base.
James Loney 1B TB 7 Months
Loney went 3-for-4 with his seventh home run of the season and three RBI in Tuesday's loss to the Tigers.
Loney drove in all three runs on a home run in the first inning off Tigers ace Max Scherzer. The 30-year-old is on a relative power binge with two long balls and five RBI over his last four games, but as a whole, he's bringing his typical high-average, good defense and minimal power profile to the table yet again this season.
James Loney 1B TB 8 Months
Loney was 3-for-5 with two RBI and a run Wednesday in a 10-2 win against the Rangers.
Wednesday was Loney's fifth multi-hit game of August. The 30-year-old doesn't fit the power profile of a first baseman, but is hitting .327 this month.
James Loney 1B TB 8 Months
Loney is out of the lineup Friday against the Cubs.
Loney has started at first base every game since July 7 for the Rays, but will give way to Sean Rodriguez for the afternoon tilt. Loney is hitting over 50 points lower against left-handed pitching, so Friday will be the perfect opportunity for a day off with southpaw Tsuyoshi Wada on the hill for the Cubs. Look for Loney to return to action Saturday.


text:
- Index
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David Beckham Ready to Play Soccer in America
David Beckham Ready to Play Soccer in America
David Beckham Ready to Play Soccer in America
Before David Beckham can make America love soccer, he has to get used to soccer in America.
Like what to call it.
It's football to the rest of the world, and the superstar from England kept getting "soccer" stuck in his throat when he was introduced Friday amid confetti and screaming fans as the Los Angeles Galaxy's new $32-million man.
"I've called it football my whole life," Beckham said, smiling. "Calling it soccer is not a problem for me. Well, at the moment it is because I keep getting it mixed up, but at some point I'll get it after a couple of weeks."
And no, Beckham said, he doesn't expect Americans to change their ways; he said he wants to adapt to his new country's lingo.
Beckham will be living in Beverly Hills and working at Home Depot - Center, that is. The Galaxy's stadium was stuffed with 5,000 fans and hundreds of reporters and photographers intent on recording every gesture and word uttered by him.
Six months of anticipation culminated with Beckham accepting his new No. 23 jersey on a stage set up on the field with cannons shooting out blue, gold and white confetti.
"It's nice to see so many fans, and I thank you for that," he told the crowd sweating under a hot sun. "Now my family have moved to Los Angeles, something we're looking forward to, something we're very proud of, and in our life everything's perfect."
The Galaxy is paying Beckham $32.5 million over five years to turn the struggling team into a winner and promote soccer in the United States, where it badly trails football - the American variety - basketball and baseball in popularity. The Galaxy is next to last in the Western Conference with a 3-5-4 record.
"I think soccer in America has a lot of potential, just maybe something is missing to take it to another level, and I'm hoping I'm going to be part of that," said Beckham, whose playing debut is set for July 21. "There's been expectations all the way through my career, and at the moment this is a big one. Hopefully, I can handle it in the right way."
There are lots of other newsworthy material surrounding Beckham and his Spice Girl wife, Victoria, and their kids as they come to America. Here are some of the wagers available in the celebrity betting section of the Bodog Sportsbook.
Bet On: Will a paparazzo be arrested for trespassing on David and Victoria Beckham's property in 2007?
Bet On: Will Victoria Beckham talk about Scientology on the premiere of the NBC special "Victoria Beckham: Coming to America"?
And, of course, you can wager on Beckham the old-fashioned way - by betting on soccer.
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text:
11/30/2012 (2 years ago)
American Center for Law and Justice (www.aclj.org/)
Our client, Frank O'Brien, is a St. Louis business owner who takes his Catholic faith seriously; so seriously that he doesn't want the government to force him to pay for things he considers immoral. More than 40 cases have been filed around the country challenging the HHS Mandate on behalf of religiously affiliated schools, charitable institutions, and nonprofit organizations who say that the Mandate is a blatant violation of the Constitution's protection of religious freedom.
American Center for Law and Justice (www.aclj.org/)
11/30/2012 (2 years ago)
Published in U.S.
Keywords: Francis J Manion, mandate, OBrien, abortion, Frank O'Brien, HHS Mandate, free exercise, religious freedom, ACLJ, Jay Sekulow, anti-Catholic, Obamacare
WASHINGTON, DC (ACLJ) - On Wednesday, the 8th Circuit Court of Appeals granted our motion for an injunction against the U.S. government's enforcement of the so-called "HHS Mandate," a series of regulations requiring virtually all employers to pay for their employees' contraception, sterilization, and early abortion-inducing drugs.
Our client, Frank O'Brien, is a St. Louis business owner who takes his Catholic faith seriously; so seriously that he doesn't want the government to force him to pay for things he considers immoral.
O'Brien doesn't care -- doesn't want to know -- what his employees do in their bedrooms. He just doesn't want Kathleen Sebelius or Barack Obama telling him he has to pay for what they do, even when doing so is against his religion.
More than 40 cases have been filed around the country challenging the HHS Mandate on behalf of religiously affiliated schools, charitable institutions, and nonprofit organizations who say that the Mandate is a blatant violation of the Constitution's protection of religious freedom.
Frank O'Brien's case was the first filed on behalf of a for-profit business owner. In September, the U.S. District Court in St. Louis threw out O'Brien's case, saying that the Mandate was not a "substantial burden" on his exercise of religion. We filed an appeal with the 8th Circuit before the ink was dry on the court's opinion.
The district court reasoned: O'Brien wasn't being forced to use contraception; he could still attend Mass; he could still send his kids to Catholic schools. What's the big deal?
The big deal is that in this country, from its founding, the right to the "free exercise of religion" has always meant much more than the mere freedom to worship within the walls of your church.
The Continental Congress, in the darkest hours of the Revolution, with the very existence of the newly birthed Nation threatened by the approach of the greatest military machine in the world, saw fit to exempt from military service "people who, from religious principles, cannot bear arms in any case." Congress didn't tell the Quaker and Moravian pacifists who asked for the exemption that they were still free to have their meetings and raise their children as they chose, so shoulder a musket and fight.
Congress told them that "this Congress intend no violence to their consciences" and exempted them from what most people in just about every country in the world would consider a paramount duty of any citizen.
That expansive idea of, "free exercise of religion," encompassing not only what a person believes, but also what a person does or refuses to do, in the public square, and yes, even in the commercial marketplace, is what the First Amendment and the Religious Freedom Restoration Act (RFRA) are meant to protect.
Nobody froze with Washington at Valley Forge to secure the right of government bureaucrats to coerce free men and women to violate their consciences. Nobody died on Omaha Beach so that someday all Americans would have the right to force their boss to buy them birth control pills.
The HHS Mandate, which compels employers to directly contribute to causes which they abhor, is, as Jefferson would put it, "tyrannical." We at the ACLJ will not stand by while this government, or any government, tries to grind the First Amendment beneath its heels.
Francis J. Manion is Senior Counsel with the ACLJ who emphasizes First Amendment law and pro-life legal matters before state and federal courts.
The American Center for Law and Justice (ACLJ) focuses on constitutional law and is based in Washington, D.C. This article is used with permission.
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Priming a Pump
Our irrigation well pump pressure was way down so we added some acidizing tablets and let it sit overnight. When I turn the pump on now to drain the acid to the field behind us there is no water coming so it seems like a need to prime it.
I've never had to prime it before and don't know how. Can someone please give me some tips on how to do it? I've attached a picture of the pump.
Thanks in advance.
Attached a hose to the faucet. turn on the hose water and open the faucet to let the water into the pump housing. When the pump housing is full, close the faucet and run the pump. If the pump is primed and working properly disconnect the hose from the faucet. You could actually leave the faucet open with the water hose running and run the pump until it is working and then shut off the faucet. Hope it works out. JMHO Aloha
The pipe in the well must have a check valve between the bottom of the well and the pump to hold the prime. Two-line systems must have the check valve at the bottom of the well. Your one-pipe system appears to have the brass check valve right up against the pump. If the pump fails to hold prime, replace that part.
Your well is probably not more than 20 feet deep. Does it have water in it now?
Bus is entirely correct. If your check valve is stuck open. You are pouring water down your well. If it is a minor leak, you can fill up your pump housing and start your pump that it will open the check valve and pull from the well. It you turn off your pump and hose and wait 1/2 hour and start your pump. If you have lost prime replace you check valve. If you did not wait an hour and check again, etc. till you determine how long it takes to lose the prime. Then replace the check valve. Place you hose in a 5-gal bucket and time how long it takes to fill the bucket. Compute you gallons per minute. Estimate the volume of the housing (cubic feet) x 7.8 14 gallons per cubic foot. Time your house to put that many gallons into the housing and start the pump and see what happens. Let us know how it goes. Aloha
I was able to get it primed and the pump was working...for one day. However, there now is a crack in the PVC on the other side of the pump where the metal meets the PVC. I'm guessing it's because the pump was not secured to the base so it could move around but I'm not sure. It's not a good sprinkling year for us.
Thanks for all of your help.


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Eula to play Morticia in 'Addams Family' musical
MANILA, Philippines – Actress Eula Valdez is returning to theater later this year after Atlantis Productions said she will be playing Morticia Addams in the musical adaptation of "The Addams Family."
|Valdez plays Morticia Addams in "The Addams Family" musical.
"We are proud to announce Eula Valdez as Morticia Addams in The Addams Family! November 2013 at the Meralco Theater," the theater group said on its Facebook page on Thursday.
Atlantis also attached a photo of Valdez made up like the character, memorably played by Anjelica Huston in the 1991 movie.
Valdez previously appeared in Atlantis' production of the Tony Award-winning musical "Nine" last year, for which she won the Best Featured Actress (Musical) prize at the 2012 BWW Philippines Awards.
"The Addams Family" is the third offering of the newly formed Viva Atlantis Theatricals, a joint venture between the theater group and entertainment outfit Viva Communications, Inc.
Viva Atlantis Theatricals will make its bow in the local theater scene with the stage musical version of the 1997 hit movie, "The Full Monty," which will open in April 2013.
This will be followed by "Tarzan: The Musical," the stage version of the hit Disney cartoon movie with music by pop superstar Phil Collins, which will open in June at the Meralco Theater.


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I've been reading up on these "coat" threads, and I cant decide if I want to try this or not. #1, I cant decide which one is the most durable. Also, can you coat stainless steel?
Can anyone help me.
Good question, bet Woody can answer it.
Like it or not, when the chips are down and lives are at stake, an armed citizen can be the "first responder." People who dont like guns invariably rely on people who have guns when their lives are in danger.
Looked into this myself. From what I read and (more importantly) saw, Ceracote looks to be the way to go.
I have used a LOT of Gunkote and its a good product. I have also used ceracoat--another good product. No matter which one you use, if you use your gun routinely you will eventually experience wear from use and holster wear. The nice part is not worrying about rust or corrosion on the coated surfaces.
One major thing to keep in mind is prep work. No matter which product you decide to use, all the work is in the preparation before you apply the coating.
I have had good experiences with gun kote on stainless, reg steel, and even some polymers using gental heat of course!!!
Good luck with your project!
I've used gunkote, duracoat, and molyresin. For metal surfaces I would go with gunkote or molyresin they are more durable. Robb is right 95% of good gun finish is prep work. Basting, sanding and finishing and parkerizing the metal depending on the metal type and tools at hand, degreasing before painting.


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Too much moss on cedar
reg_pnw7(WA 7, sunset 4)April 1, 2012
Where I live, moss grows on anything that stands still for more than 5 minutes. I have a bonsai'd blue atlas cedar with a lot of moss growing on the branches. To the point where the moss is obscuring the branching pattern, such as it is. I like moss on trees, but this seems a bit much. I know I can't get rid of the moss, but do you all think I should try trimming it back, or just leave it alone and resign myself to a bonsai of arboreal moss?


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Town Square
Stanford educated Prince Philippe ascends to Belgian throne
Original post made by Nayeli, Midtown, on Jul 21, 2013
Comments (3)
a resident of Midtown
on Jul 21, 2013 at 9:36 am
Crown Prince Philippe ascended to the throne after his father, King Albert II, officially abdicated today due to health reasons.
Philippe attended graduate school at Stanford during the 1980s and graduated with a Master of Arts degree in Political Science.
a resident of Another Palo Alto neighborhood
on Jul 22, 2013 at 1:10 pm
Bon chance, Philippe! You have your hands full with the country about to split in two!
a resident of Crescent Park
on Jul 25, 2013 at 11:22 am
bru is a registered user.
The outdated institution of royalty is something that should go away.
Keeping royalty around is like maintaining a small plantation of slaves as a memorial to times past, and is completely something that should go away.
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29 Mar 2015
By Julia Halperin. Web onlyPublished online: 12 April 2014
The demolition of the American Folk Art Museum's former home is due to begin within the month despite protests from architects, preservationists and critics. The Museum of Modern Art (MoMA), New York, which purchased the building in 2011 after the folk art museum defaulted on its debt, plans to raze it in order to accommodate its expansion, expected to open by 2018.
Last week, the museum filed plans with New York's buildings department to conduct a "partial demolition" of the building, as well as other construction work, for $1.6m, according to the New York Daily News. Building crews are scheduled to begin erecting scaffolding and protective netting on the structure on Monday 14 April. The process is expected to last about two weeks and deconstruction will follow. The demolition work is due to be complete by this summer, according to a MoMA spokeswoman.The decision to demolish the American Folk Art Museum building, which was designed by Tod Williams and Billie Tsien Architects in 2001, caused such a ruckus when it was first announced in 2013 that MoMA asked the architecture firm Diller Scofidio & Renfro to take a second look at the plans and see if it could be avoided. In January, the architects announced they had found no alternative. "You pass a tipping point where there's not enough of the original structure to actually maintain its identity," the architect Elizabeth Diller told the New York Times at the time. MoMA has said that it intends to preserve the 63 unique bronze panels that comprise the building's 82ft-tall façade. Construction crews are expected to remove them one by one before demolition begins, though the objects are "not entering MoMA's collection, and no decision has been made at this point as to future plans", a spokeswoman says.
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More than a quixotic effort, I designed my Iconic Horizontal Yellow Hybrid building for the permanent collection early last spring that would even integrated the Folk Art Building & tried mightily to have MoMA adopt it as the way forward. 1000 times beyond the horror of what's to be. MoMA didn't relish the idea of mine -- even Blocked me from leaving comments on it's Facebook page after posting mine & describing it's virtues. MoMA didn't relish mine -- even the idea was too much. MoMA would brook no opposition or consider an alternative to other than what it wanted. The original architects provided me cut away isometrics.
What is the future of the collection? It has some real jewels.
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What is the future of the collection? It has some real jewels....
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