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MTA Introduces Baby on Board Buttons for Expecting Mothers and Elderly, Disabled
The MTA has announced new "Baby on Board" buttons as part of a pilot for the Courtesy Counts campaign that can be worn by expecting mothers in the NYC subway.More
The MTA has announced new "Baby on Board" buttons as part of a pilot for the Courtesy Counts campaign that can be worn by expecting mothers in the NYC subway.More
Step into the past with this photographic exhibit of the deconstruction of the Third Avenue Elevated Line in NYC at the Transit Museum in Grand Central TerminalMore
Following a ceremonial ride yesterday with Mayor Bill de Blasio (watch our live feed of the trip here), the NYC Ferry launched officially this morning at 5:30 AM. The initial launch will cover two routes: Rockaways – Sunset Park – Wall Street, and East River, folding in the East River Ferry service into the new NYC Ferry …More
This morning, we are on the ceremonial first trip on the NYC Ferry, which opens officially May 1st. Following up our inside look inside the ferry vessels before they got their US Coast Guard stamp of approval on Thursday, this time we rode with Mayor Bill de Blasio, Queens Borough President Melinda Katz, community leaders and …More
10 fun facts we learned at the grand opening of the Kosciuszko Bridge, where we heard Brooklynites and Queens residents collectively release a sigh of relief.More
Photos from today's grand opening of the new Kosciuszko Bridge between Brooklyn and Queens, with Governor Cuomo crossing the span in FDR's 1932 Packard car.More
We got a sneak peek on the NYC Ferry, before the system officially launches Monday, May 1st. Five boats were docked at the shipyard in the Brooklyn Navy Yard.More
NYC Ferry Operated by Hornblower will bring new connections to our city of water. To mark the event, we're looking at four times when ferries saved the day.More
In a "Post-Moses New York," we can reexamine how we invest in public transit infrastructure to build a system that can efficiently move people around.More
Mayor Gregor Robertson calls the Arbutus Corridor "Vancouver's chance to have a New York-style High Line," the successful park on Manhattan's West Side.More
The first of the Citywide Ferry vessels has left Horizon Shipyard in Alabama on its maiden journey to NYC around Florida and up to the Atlantic Ocean..More
The highly anticipated launch of Citywide Ferry Service this summer will redefine how New Yorkers explore and experience the East River waterfront.More


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Winger Andre Schurrle failed to threaten in an unfamiliar centre-forward role in Paris and is a relative outsider at 13/5 (3.60) with Paddy Power to find the net, or a lengthy 15/2 (8.50) to break the deadlock.
|Goalscorer Special
|Odds from Paddy Power
|Cavani to score anytime
|Hazard to score anytime
|Torres to score anytime
|Schurrle/Lavezzi to score anytime
|Pastore to score anytime
|Eto'o to score first
Mourinho must, therefore, be praying that Samuel Eto'o will be fit enough to take to the field, with the Cameroonian representing a much more reliable presence in front of goal.
The Portuguese boss admitted he was prepared to take a risk on the 33-year-old, who has not played since opening the scoring in last month's big win over Arsenal, meaning odds of 11/2 (6.50) could prove a solid investment on him getting the ball rolling for a fourth consecutive appearance.
Otherwise, the Blues may be forced to rely yet again on a midfield that provided all three goals in Saturday's win over Stoke, even without the rested Eden Hazard.
The Belgian talisman scored his side's only goal in Paris from the penalty spot and offers possibly their biggest threat once again this evening, with odds of 15/8 (2.88) on him getting on the score sheet well worth considering.
One key headline from the first leg in France was the injury to Zlatan Ibrahimovic that rules the irrepressible Swede out of tonight's encounter, although Laurent Blanc is not short of backup for the trip to London.
Having been shifted out to the right wing to make space for Ibrahimovic, Edinson Cavani proved within 43 minutes against Reims on Saturday what he is capable of when leading the line and looks like solid value at 9/5 (2.80) to strike once again against a home team chasing the game.
Elsewhere, the likes of Ezequiel Lavezzi 13/5 (3.60), Javier Pastore 10/3 (4.33) and Lucas Moura 7/2 (4.50) are bound to ensure a long night for the home defence.
|Cavani to score anytime for a 2pt stake at 9/5 (2.80) with Paddy Power
|Eto'o to score first for a 1pt stake at 11/2 (6.50) with Paddy Power
Sign up with Paddy Power for up to £250 in free bets
Al Hain-Cole is an experienced tipster and avid follower of European football. He specialises in accumulators and if you would like to read more from Al you can follow him on Twitter here.

subset: commoncrawl


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Rococo style extra long door plate with lock face plate to cover hole. Can be fitted with actual dead bolt lock if desired.
The dimensions are: 17.625 in. H x 3.5 in. W, 1.5 lbs
**NOTE: Before purchasing directly through PayPal, please inquire about item availability and please wait for invoice to be emailed to you BEFORE paying directly. Often, an item has been sold quickly & not taken off yet or shipping prices have to be adjusted. Thank You!
Your source for Architectural Antiques & Altered Antiques
Industrial, altered antiques, doors, hardware, farm tables, tin mirrors and panels and mantels.


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GraphicRiver Market Cloud Logo Templates 6251484
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GraphicRiver Market Cloud Logo Templates 6251484
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High fructose intake has been linked to insulin resistance and cardiac pathology. Dietary fructose-induced myocardial signaling and morphological alterations have been described, but whether cardiomyocyte function is influenced by chronic high fructose intake is yet to be elucidated. The goal of this study was to evaluate the cardiomyocyte excitation-contraction coupling effects of high dietary fructose and determine the capacity for murine cardiomyocyte fructose transport. Male C57Bl/6J mice were fed a high fructose diet for 12 wk. Fructose- and control-fed mouse cardiomyocytes were isolated and loaded with the fura 2 Ca2+ fluorescent dye for analysis of twitch and Ca2+ transient characteristics (4 Hz stimulation, 37°C, 2 mM Ca2+). Myocardial Ca2+-handling protein expression was determined by Western blot. Gene expression of the fructose-specific transporter, GLUT5, in adult mouse cardiomyocytes was detected by real-time and conventional RT-PCR techniques. Diastolic Ca2+ and Ca2+ transient amplitude were decreased in isolated cardiomyocytes from fructose-fed mice relative to control (16 and 42%, respectively), coincident with an increase in the time constant of Ca2+ transient decay (24%). Dietary fructose increased the myofilament response to Ca2+ (as evidenced by a left shift in the shortening-Ca2+ phase loop). Protein expression of sarcoplasmic reticulum Ca2+-ATPase (SERCA2a), phosphorylated (P) phospholamban (Ser16), and P-phospholamban (Thr17) was reduced, and protein phosphatase 2A expression increased, in fructose-fed mouse hearts. Hypertension and cardiac hypertrophy were not evident. These findings demonstrate that fructose diet-associated myocardial insulin resistance induces profound disturbance of cardiomyocyte Ca2+ handling and responsiveness in the absence of altered systemic loading conditions.
- excitation-contraction coupling
- cardiac
- myocardial
- cellular
in western societies, the use of added sweeteners has increased by 25% during the last 30 years, and it has been estimated that the average adolescent (North American) consumes over 30% of energy intake in the form of added sugars (17, 29). Fructose intake has been identified as a significant risk factor for insulin resistance and cardiovascular disease, independent of body mass index (45). Experimental models have demonstrated that a high fructose diet disturbs metabolic homeostasis, increases plasma fructose, and induces systemic insulin resistance in rodents (2, 24, 32, 35). The existence of an insulin-resistant cardiomyopathy, associated with perturbed cardiac metabolism and functional impairment, is generally recognized (33, 46, 48). In a previous study, we have demonstrated that excess fructose intake is associated with elevated blood glucose, glucose intolerance, and normal plasma insulin in the absence of hypertension and obesity (35). We have also shown that fructose feeding induces diffuse myocardial fibrotic infiltration linked with suppressed cardiomyocyte viability signaling (35). The impact of elevated dietary fructose intake on cardiomyocyte functional performance is yet to be demonstrated.
Cellular fructose uptake is mediated by insulin-independent transporters. Fructose is rapidly phosphorylated by fructokinase and bypasses the glycolytic rate-limiting enzyme, phosphofructokinase, proceeding through glycolysis to produce pyruvate and lactate in a less-controlled manner than glucose (30). The close association of glycolytic enzymes with Ca2+-related transporters provides indication that specific excitation-contraction coupling processes are particularly reliant on glycolytically produced ATP (38, 50). There is some evidence that high fructose intake suppresses cardiac output in vivo (9), but cardiomyocyte functional effects of dietary fructose have not been directly assessed. The combined insults of myocardial insulin resistance-induced metabolic alterations and direct fructose-induced glycolytic dysregulation may have specific consequences for cardiomyocyte function. Rodent models of insulin-resistant cardiomyopathy (e.g., db/db mice, ob/ob mice, high-fat-fed rodents) exhibit cardiomyocyte excitation-contraction coupling disturbances coincident with hypertension and/or obesity (5). The load-independent myocardial functional effects of insulin resistance are not yet delineated.
We have recently demonstrated that fructose feeding in mice increases myocardial reactive oxygen species (ROS) production and downregulates the insulin-responsive phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway, independent of hypertension and obesity (31, 35). This signaling dysregulation was linked with myocardial structural pathophysiology. Other studies have previously identified a role for Akt in cardiomyocyte Ca2+ regulation, specifically phosphorylating key Ca2+-handling proteins, the L-type Ca2+ channel (8, 27) and phospholamban [PLB; the sarcoplasmic reticulum Ca2+-ATPase (SERCA2) regulator] (7). Activity of Ca2+ flux proteins is tightly regulated by both kinase and phosphatase activities, and there is some evidence that dephosphorylation of PLB and ryanodine receptors (14) plays a role in diabetic cardiomyopathy (39). No study to date has sought a link between increased fructose intake and cardiomyocyte Ca2+ dysregulation in the insulin-resistant myocardium.
Given the regulatory associations between insulin signaling, glycolysis, ROS, and cardiomyocyte excitation-contraction coupling, we hypothesized that fructose dietary intervention would directly modulate cardiomyocyte Ca2+ handling and contractile performance, in the absence of systemic loading disturbance. To examine this contention, mice were subjected to a high fructose diet intervention for 12 wk. Isolated cardiac myocytes were loaded with a Ca2+-sensitive fluorophore for functional assessment. Expression and signaling studies of key transporters involved in Ca2+ flux regulation were undertaken. This investigation provides the first demonstration that a relatively short-term elevation of fructose intake in mice induces profound disturbance of cardiomyocyte Ca2+ handling and Ca2+ responsiveness.
Dietary treatments and in vivo measurements.
Male C57Bl/6J mice were housed in temperature-controlled conditions in a 12:12-h light-dark cycle and were cared for in accordance with the "Principles of laboratory animal care" (NIH publication no. 85–23, revised 1985; http://grants1.nih.gov/grants/olaw/references/phspol.htm) and the Australian Code of Practice for the Care and Use of Animals for Scientific Purposes, and procedures were approved by the Animal Ethics Committee of the University of Melbourne. At the commencement of the dietary treatment period, mice aged 4–5 wk were allocated to either a control (54% starch, 10% sucrose, 7% total fat, and 19.4% protein) or high fructose (60% fructose, 3.6% starch, 7% total fat, and 19.4% protein) diet, as previously detailed (31). The diets were based on the American Institute of Nutrition standard rodent growth diet (40), were of equal digestible energy, and were micro- and macronutrient matched (AIN93G, SF03–018; Specialty Feeds, WA, Australia). Measurement of blood glucose was performed following a 6-h fast in the final week of dietary intervention. A small blood sample was obtained by tail prick, and glucose was determined by a blood glucometer (ACCU-CHEK Advantage; Roche, Mannheim, Germany). We have previously demonstrated that 12 wk of 60% fructose feeding induces significant glucose intolerance (∼14% increase in area under the glucose tolerance curve), with maintenance of normal blood pressure (35).
Tissue recovery.
At the completion of the 12-wk feeding period (age 16 wk), all mice were fasted for 3–4 h, heparinized (100 IU ip), and anesthetized by sodium pentobarbitone (100 mg/kg ip). Hearts were excised and weighed for measurement of cardiac weight indexes (cardiac weights normalized to tibia length). Hearts were utilized for myocyte isolation or assigned to molecular analysis (Westerns, real-time RT-PCR).
Cardiomyocyte isolation.
Ventricular cardiomyocytes were isolated from fructose- and control-fed mice (18). Following heart excision, the aorta was cannulated, and the heart was retrogradely perfused with Ca2+-free HEPES-buffered Krebs (in mM: 150 NaCl, 5 KCl, 0.33 NaH2PO4, 1 MgCl2, 25 HEPES, 20 d-glucose, 3 sodium pyruvate, and 1 sodium lactate, pH 7.4) at 2 ml/min at 37°C for 10 min. Addition of Type II Collagenase (0.66 mg/ml, 295 U/mg; Worthington Biochemicals), CaCl2 (50 μM), and trypsin (33 μg/ml; Sigma-Aldrich) to the perfusate enabled heart digestion. The heart was then removed from the cannula, atria were dissected away, and the ventricles were gently teased apart. Cells were dispersed in a high-potassium HEPES-buffered Krebs solution (in mM: 30 KCl, 90 KOH, 30 KH2PO4, 3 MgSO4, 50 glutamate, 20 taurine, 0.5 EGTA, 10 d-glucose, and 10 HEPES, pH 7.4) and resuspended in Ca2+-free HEPES-buffered Krebs with trypsin inhibitor (25 μg/ml; Sigma-Aldrich).
Cardiomyocyte Ca2+ handling and twitch analysis.
Cardiomyocytes were loaded with the Ca2+ fluorescent dye fura 2-AM (1 μM, 20-min incubation at 25°C; Invitrogen). The fura 2 loading conditions provided an optimal signal-to-noise ratio without compromising myocyte inotropic status and responsiveness. Myocytes were superfused with 2 mM Ca2+-HEPES buffer (in mM: 146.2 NaCl, 4.69 KCl, 11 d-glucose, 0.35 NaH2PO4H2O, 1.05 MgSO47H2O, and 10 HEPES) and stimulated to establish steady-state contractile performance at 4 Hz (>5 min, 37°C). At these near-physiological conditions, myocyte contractions were stable, and no evidence of spontaneous Ca2+ release was observed. Myocyte Ca2+41). The indexes used to describe the Ca2+ transient were amplitude [ratio of fluorescence at 360 to 380 nm (F360:380)], diastolic Ca2+ (F360:380), systolic Ca2+, time constant of decay (tau, ms), and the area of the Ca2+ 2+-shortening phase-loop plots were constructed as described (3, 44).
Western blot analysis of myocardial protein expression.
Frozen cardiac tissue was homogenized in 100 mM Tris·HCl, 5 mM EGTA, 5 mM EDTA (Sigma-Aldrich), protease inhibitors, and phosphatase inhibitors (Roche, Basel, Switzerland). Sample protein concentration was determined by a modified Lowry assay (37). Protein expression was determined by SDS-PAGE and Western blotting. Equal protein loading was confirmed by staining the polyvinylidene difluoride membranes with Ponceau-S (Sigma-Aldrich). Membranes were incubated with primary antibody overnight at 4°C. Primary antibodies were sourced as follows: SERCA2a (no. A010-20) and phospho(Thr17)-PLB (no. A010-13) (Badrilla, Leeds, UK); phospho(Ser16)-PLB (no. 07-052) and PLB (no. 05-205) (Upstate); phospho-calmodulin kinase (CaMK) II (no. ab32678) (Abcam, Cambridge, UK); β-tubulin, protein phosphatase 2A (PP2A)-A subunit, and PP2A-C subunit (Cell Signaling Technology). Membranes were incubated for 1 h with anti-rabbit or anti-mouse horseradish peroxidase-conjugated secondary antibody (GE Healthcare, Buckinghamshire, UK). The ECL Plus (Amersham; GE Healthcare) chemiluminescent signal was imaged and analyzed using Quantity One software (Bio-Rad).
RNA was extracted from frozen cardiac tissues using the TRIzol reagent in conjunction with the PureLink Micro-to-Midi Total RNA Purification kit (Invitrogen) as per the manufacturer's instructions and was reverse transcribed using the SuperScript III First-Strand Synthesis System (Invitrogen). Real-time RT-PCR was used to determine the relative gene expression levels of β-myosin heavy chain (β-MHC), α-myosin heavy chain (α-MHC), sodium/hydrogen exchanger (NHE), solute carrier family 2 facilitated glucose/fructose transporter member 5 (Slc2a5, GLUT5), and the housekeeper gene 18S in ventricular tissue. Real-time RT-PCR primer sequences for each gene were as follows; β-MHC: 5′-TCTCCTGCTGTTTCCTTACTTGCTA-3′ and 5′-GTACTCCTCTGCTGAGGCTTCCT-3′; α-MHC: 5′-GCCCAGTACCTCCGAAAGTC-3′ and 5′-GCCTTAACATACTCCTCCTTGTC-3′; NHE: 5′-AGC TGG AGC AGA AGA TCA CCA-3′ and 5′-AGG TCT GCC TTG GGT TCA TAG-3′; GLUT5 (Slc2a5): 5′-CCAATATGGGTACAACGTAGCTG-3′ and 5′- GCGTCAAGGTGAAGGACTCAATA-3′; and 18S: 5′-TCGAGGCCCTGTAATTGGAA-3′ and 5′-CCCTCCAATGGATCCTCGTT-3′. The comparative ΔΔCt method was used to analyze the genes of interest as described (26, 31). To confirm the presence of the fructose-specific transporter, GLUT5 (Slc2a5), in adult mouse isolated cardiomyocytes and heart homogenate, conventional RT-PCR was performed using Platinum Taq Polymerase (Invitrogen) with two consecutive runs of 30 PCR cycles to allow visualization of low-expression genes. Conventional RT-PCR primer sequences, designed to obtain an amplicon size of 492 bp, were as follows: GLUT5, 5′-CCAATATGGGTACAACGTAGCTG-3′ and 5′-AACTGGCCAGCCATCCTCATTT-3′.
Statistical analyses.
Data are expressed as means ± SE and were analyzed with Student's unpaired t-test. A P value <0.05 was considered statistically significant. Graphs were created, and statistical analyses were performed using GraphPad Prism version 5.02 (GraphPad Software). For analysis of Western immunoblots, individual control values (densitometric data: arbitrary units) were normalized to the mean of the control group to enable the variability of this group to be presented in the fold change data.
Morphological characteristics of fructose-fed mice.
At the completion of the 12-wk fructose-feeding intervention, blood glucose concentrations were increased by 20% in fructose-fed mice relative to control. No significant differences were observed in total heart mass or ventricular mass between treatment groups (Table 1). Because fructose-fed animals showed a small relative reduction in body weight gain during the treatment period, cardiac tissue measures were normalized to tibial length, which was similar for both groups. Cardiac weight index and ventricular weight index were not altered by fructose feeding. These findings are consistent with our previous report that cardiac hypertrophy is not evident at the whole heart or cellular level (35) and confirm the absence of myocardial tissue hypertrophy with an identical mouse fructose feeding regime.
Anomalous cardiomyocyte Ca2+ handling and contractile performance in fructose-fed mice.
The Ca2+ transients recorded from myocytes of fructose-fed mice contrasted dramatically with those recorded from control myocytes, as the representative traces presented in Fig. 1A demonstrate. The mean transient amplitude was 42% reduced in fructose-fed cardiomyocytes relative to controls (1.39 ± 0.15 vs. 2.39 ± 0.46 F360:380, P < 0.05, Fig. 1B). Diastolic and peak systolic Ca2+ levels were both significantly lower in myocytes of fructose-fed mice (Fig. 1, C and D). Furthermore, fructose feeding increased the time constant of transient decay (tau) by 24%, indicative of delayed Ca2+ removal from the cytosol during twitch relaxation (Fig. 1E). No difference in time to peak transient was observed (fructose: 16.8 ± 0.8 ms vs. control: 17.2 ± 0.6 ms). The fructose-induced Ca2+ transient alterations were coincident with a 37% decrease in the area under the transient (Fig. 1F).
In contrast, no significant differences could be detected in the shortening profiles of cardiomyocytes of fructose- and control-fed animals, and these twitch records were indistinguishable (Fig. 2A). Mean resting (diastolic) cardiomyocyte length was not different between groups (Fig. 2B), indicating similarity of myocyte size, coincident with maintained tissue mass. As depicted in Fig. 2, C–F, mean peak shortening attained (%shortening) and maximum rates of shortening and lengthening (%MRS, %MRL) were similar for both myocyte groups, and the duration of the twitch cycle was not altered by the high fructose diet. Thus, the contractile performance of cardiomyocytes of fructose-fed mice was not diminished, even though significant reduction in systolic and diastolic Ca2+ transient characteristics was observed. Mechanistic exploration of this twitch-transient anomaly was pursued.
Increased myofilament Ca2+ responsiveness in fructose-fed mouse cardiomyocytes.
Evidence of altered Ca2+ responsiveness in cardiomyocytes of fructose-fed mice was sought. Examination of individual myocyte shortening-Ca2+ relationships was undertaken using "phase-loop" plots (44). These plots map myocyte Ca2+ levels against cell length (normalized to diastolic cell length) throughout the contraction and relaxation phases of the activation cycle. During the relaxation phase, the descending portion of the "loop" provides a dynamic index of myofilament Ca2+ sensitivity (3, 44). Exemplar myocyte Ca2+-shortening phase-loop plots, presented in Fig. 3A, show a left shift in the relaxation phase in the fructose group compared with control, indicative of increased myofilament responsiveness to Ca2+ (44). The phase-loop shift was quantified by assessment of intracellular Ca2+ at 50% myocyte relaxation. Fructose-fed mouse cardiomyocytes exhibited a 22% decrease in Ca2+ levels at 50% myocyte relaxation relative to controls (Fig. 3B). These data are consistent with increased myofilament Ca2+ responsiveness.
Myofilament shortening response to Ca2+ is substantially determined by myosin isoform type (α- vs. β-MHC) and by intracellular pH. An increase in the relative expression of α- to β-MHC isoform is associated with increased myofilament Ca2+ sensitivity (36). The mRNA expression levels of MHC isoforms were compared in fructose- and control-fed mouse hearts. A marked and significant increase in the α-MHC-to-β-MHC mRNA ratio (Fig. 3C) was detected in fructose-fed mouse myocardium (2.8-fold increase), which would indicate increased myosin responsiveness to Ca2+.
Intracellular pH modulates myofilament Ca2+ sensitivity (10), and altered proton efflux through upregulation of NHE-1 has been previously observed in association with myocardial insulin resistance (13). The effect of fructose feeding on NHE-1 expression was evaluated, and no difference between treatment groups in relative transcript levels for this transporter was detected (Fig. 3D). These findings suggest that myofilament MHC isoform, but not NHE-1-mediated proton flux, plays a role in increasing the Ca2+ responsiveness of cardiomyocytes of fructose-fed mice.
Myocardial Ca2+-handling proteins are downregulated in fructose-fed mice. To evaluate the basis for the fructose-induced alterations in cardiomyocyte Ca2+ transients, additional molecular analyses were undertaken. Ca2+ removal from the cytosol during relaxation is primarily mediated by SERCA2a in cardiomyocytes. As depicted in Fig. 4A, myocardial protein expression of SERCA2a was significantly decreased in fructose-fed mice, relative to control. Phosphorylation of the SERCA2 regulator, PLB at Ser16 or Thr17 residues [by protein kinase A (PKA) or CaMKII, respectively], relieves SERCA2 inhibition. Fructose-fed mice exhibited a significant reduction in the ratio of phosphorylated (Ser16) to total PLB. The ratio of phosphorylated (Thr17) to total PLB was also significantly decreased (Fig. 4C), and this was associated with a nonsignificant reduction in the level of phosphorylated CaMKII (Thr286) (P = 0.09, Fig. 4D). No effect of fructose on total PLB protein content was observed (fructose: 0.98 ± 0.16-fold change control, P > 0.05). PP2A dephosphorylates PLB at both Ser16 and Thr17 phosphorylation sites (28). PP2A subunits A (structural) and C (catalytic) were upregulated in fructose-fed mouse hearts (Fig. 5, A and B). These findings indicate that the myocardial protein density and activity of SERCA2a was downregulated in response to high fructose intake, consistent with the observation that the removal of Ca2+ from the cytosol is delayed (increased tau, Fig. 1E).
GLUT5 fructose transporter is expressed in cardiomyocytes.
To evaluate cardiomyocyte capacity for fructose uptake, expression of GLUT5 (Slc2a5) in adult mouse cardiomyocytes was determined. Real-time RT-PCR analysis demonstrated GLUT5 expression in mouse cardiomyocytes. Initial fluorescence for amplified GLUT5 PCR product was ∼18–20 cycles for mouse cardiomyocytes and 22–24 cycles for mouse heart homogenate (Fig. 6A), indicating that cardiomyocytes are the primary cell type expressing GLUT5 in cardiac tissue. Initial fluorescence for GLUT5 in mouse small intestine tissue was detected at ∼12–14 cycles (Fig. 6A). Reverse transcription "negative" and "no template control" samples did not amplify in PCR reactions. The melt curve, generated by progressive temperature increase to 95°C post-PCR amplification, revealed a single peak for GLUT5 samples, indicating high PCR product purity (data not shown). Figure 6B presents the conventional RT-PCR gel image of the GLUT5 PCR product band at 492 bp in mouse cardiomyocyte samples. Mouse small intestine represents a positive control. No evidence of the 492-bp product was observed in the negative control. Given previous reports of substrate regulation of GLUT5 in noncardiac tissues (11), the gene expression of GLUT5 in response to a 12-wk high fructose diet was examined. Real-time RT-PCR demonstrated that GLUT5 gene expression was similar in fructose- and control-fed mouse hearts (Fig. 6C).
This study provides the first evidence that high fructose intake profoundly alters cardiomyocyte Ca2+ handling and Ca2+ responsiveness. Ventricular myocytes isolated from mice subjected to a limited-duration 12-wk fructose feeding intervention exhibited dramatically reduced Ca2+ transient amplitude and lower diastolic Ca2+. Examining the underlying mechanisms involved, we have shown that suppressed Ca2+ transient amplitude is linked with a reduced level of SERCA2a. Decreased phosphorylation of the pump regulator PLB at both PKA and CaMKII target sites was demonstrated, combined with increased dephosphorylation capability of phosphatase PP2A, which targets PLB. Paradoxically, these Ca2+ perturbations were observed in the absence of discernible alterations in the myocyte twitch characteristics. By quantifying the dynamic relationship between myocyte Ca2+ levels and shortening, it was possible to identify a compensatory increase of Ca2+ responsiveness as the likely outcome of an α- to β-MHC isoform expression shift. Drawing on our previous work with this model, we have strong evidence to make the case that these molecular mechanisms can be attributed to increased myocardial ROS production and Akt signaling downregulation occurring as a consequence of myocardial insulin resistance.
The compelling finding is that, despite marked reduction in cardiomyocyte systolic Ca2+ availability induced by fructose feeding, a major adaptive increase in Ca2+ responsiveness allows myocytes to preserve peak shortening, at least for this relatively short duration of dietary treatment. With ongoing dietary exposure (or with additional coincident morbidity factors, i.e., hypertension), this adaptive capacity would be expected to reach a limit, precipitating cardiac functional demise. The biological and potential clinical importance of these findings is that significant underlying cellular excitation-contraction coupling disturbance may occur before cardiac functional impact is observable in vivo (or ex vivo) with high fructose intake. The capacity for direct fructose involvement in potentially mediating some of these actions was identified in our study by demonstration of fructose-specific transporter GLUT5 (Slc2a5) expression in murine cardiomyocytes.
Establishing cardiac- and cardiomyocyte-direct actions of high fructose intake.
In other rodent type 2 diabetic models, cardiomyopathy has been observed, generally coincident with pressure or volume loading from hypertension or obesity (5). With our model, we are positioned to evaluate cardiac functional effects without confounding load influence. Our evidence indicates that high dietary fructose intake is primarily exerting a direct effect on the myocardium and cardiomyocytes (at least in the early stages of the cardiopathology). The marked myocardial structural and Ca2+-handling disturbances are observed in the context of rather moderate systemic perturbation, i.e., no hyperinsulinemia and no hemodynamic loading. The finding that cardiomyocytes express the GLUT5 fructose transporter supports the contention that myocyte fructose entry may have a role in directly modifying metabolic signaling pathways and fueling excitation-contraction coupling. We have previously reported that insulin resistance is evidenced in this model at a myocardial level by downregulation of the insulin-responsive PI3K/Akt pathway (35). The cardiac-specific signaling alterations identified with this dietary intervention may potentially contribute to excitation-contraction coupling modulation, and we now also identify the possibility of cardiac impact contingent on tissue fructose uptake. Further work is required to fully dissect the direct and indirect myocardial effects of dietary fructose.
Murine cardiomyocytes have fructose transport capacity.
The present study is the first to demonstrate the presence of the fructose-specific transporter GLUT5 in murine cardiomyocytes. We have recently demonstrated that isolated rat cardiomyocytes have the capacity to utilize exogenously supplied fructose (34). In vitro fructose supplementation is able to abrogate the functional deficits induced by cardiomyocyte treatment with the glucose metabolic inhibitor 2-deoxyglucose. Together these studies indicate the presence of an operational cardiomyocyte fructose GLUT5 transporter.
Plasma fructose concentrations are elevated in response to high dietary fructose intake (2, 25), and increased fructose availability has been shown to induce GLUT5 expression in gut epithelial cell types (11). In contrast, we found no evidence of fructose feeding-induced cardiac GLUT5 expression upregulation in cardiac tissue. It is probable that, with elevated extracellular fructose levels, GLUT5 activity is increased, and this possibility requires investigation. Our previous work identified elevated myocardial ROS production associated with fructose feeding, consistent with dysregulated phosphofructokinase-bypass fructose metabolism (31, 35). These findings provide the impetus for further work to characterize the role of cardiac fructose uptake and metabolism in dietary fructose-induced cardiac pathology.
Ca2+-handling abnormalities in myocytes of fructose-fed mice.
There has been no previous evaluation of the impact of a high fructose diet on cardiomyocyte functional status. Our investigation reveals a marked disturbance of Ca2+ handling, apparent after a limited-duration feeding intervention of 12 wk. Ca2+ reuptake into the sarcoplasmic reticulum (SR) was impaired, as evidenced by prolonged decay of cytosolic Ca2+ during the relaxation phase. Ca2+ decay during relaxation is primarily mediated by the ATP-dependent SERCA2 pump, regulated by PLB. Reduced SERCA2a protein expression coincident with increased inhibition (due to suppressed PLB phosphorylation at both Ser16 and Thr17 sites) was demonstrated in fructose-fed mouse hearts and would be expected to induce Ca2+ transient prolongation. The observed increase in PP2A protein expression (the structural and catalytic subunits) is also consistent with decreased phosphorylation of PLB, and further work utilizing a coimmunoprecipitation approach is now warranted. CaMKII targets the PLB Thr17 site, and a significant reduction in phosphorylated-CaMKII was not detected (although a downregulation trend was evident, Fig. 4D). SERCA2 suppression mediated through Akt downregulation and PLB (Thr17) phosphorylation decrease has also been demonstrated (7) and would be expected to be operative in this insulin-resistant environment. Collectively, these influences on SERCA2 regulation are consistent with decreased SR Ca2+ loading, marked diminution of the systolic Ca2+ transient, and lower cardiomyocyte operating Ca2+ levels. Decreased Ca2+ influx via the L-type Ca2+ channel is probable, as has been recently demonstrated in myocytes from a different model of insulin resistance (13), but this has not been measured in the present study. Reduced diastolic Ca2+ levels could be partially ascribed to lower SR diastolic Ca2+ leak, and it is also feasible that fructose may facilitate subcellular local glycolytic support of Na+-K+-ATPase-coupled Na+/Ca2+ exchange, which would minimize diastolic Ca2+ levels (38, 47). Measurement of SR load level, and electrophysiological interrogation of Ca2+ fluxes modified by high fructose exposure, is now required.
Molecular mechanisms for maintaining cardiomyocyte contractile performance despite Ca2+-handling abnormalities.
Cardiac functional effect of dietary fructose has been evaluated previously using in vivo echocardiography in rodents. Inconsistent findings have been reported, both lack of functional effect [8-wk treatment (10, 43)] and performance decrement [2-wk treatment (9)]. These discrepancies may reflect differential levels of coincident hypertension and fibrotic pathology and the extent to which myocyte compensatory responses allow for maintenance of cardiac function, even when there is progressive underlying abnormality of excitation-contraction coupling. In vitro fructose manipulation in a cell culture setting has demonstrated an effect of 24-h fructose exposure on cardiomyocyte function (41). No previous study has investigated the effect of in vivo chronic high fructose on cardiomyocytes isolated from fructose-fed animals. In this study, a significant alteration in Ca2+ transients was observed without coincident effect on cardiomyocyte twitch function. These findings contrast with previous reports of cardiomyocyte contractile dysfunction in sucrose-fed mice (12, 49) and may reflect the different systemic and cardiovascular phenotype induced by sucrose and fructose diets. High sucrose diets have been reported to induce hyperinsulinemia and hypertension with normal glucose levels (12, 15, 49), whereas the fructose-fed mouse model employed in the present study exhibits normal insulin levels, hyperglycemia, and no change in blood pressure (35).
Given the major reduction in myocyte Ca2+ transient amplitude induced by high fructose intake, the observed lack of effect on myocyte contractile performance was conspicuous. Based on the shift in the Ca2+-shortening phase-loop plot, our findings indicate that increased myocyte Ca2+ responsiveness compensates for Ca2+ signal reduction to maintain contractile function. At a molecular level, at least part of the underlying mechanism involves an increase in the α-MHC-to-β-MHC expression ratio. The α-MHC isoform is associated with higher ATPase activity, increased cross-bridge kinetic, and enhanced Ca2+ sensitivity (3, 16, 36). An expression shift to increase the relative level of α-MHC seems paradoxical in a setting of tissue insulin resistance, potentially limiting glucose supply. It is generally considered that a shift to increased β-MHC expression is an "economical" adaptation, given the ATP requirements of the two isoforms. However, data from transgenic animals have shown that moderate α-MHC isoform expression can be beneficial in stress states, suggesting that a relative increase in the α-MHC-to-β-MHC expression ratio may represent a strategic outcome that compensates for the higher energy utilization of this isoform (19). In the present study, cardiomyocyte contractility was maintained in fructose-fed mice despite dramatic reductions in Ca2+ transient amplitude. It is well established that the α-MHC-to-β-MHC expression ratio is linearly correlated with power output in isolated myocytes and intact hearts (1, 23). Thus the observed increase in α-MHC/β-MHC expression may allow for contractility maintenance by offsetting the reduction in activator Ca2+ available to the myofilaments. In this study, the MHC isoform shift was characterized at the mRNA level. This approach has been previously validated in a rodent model of hypertensive cardiopathology (43). A more detailed dissection of the contribution of MHC isoform switch to myofilament Ca2+ responsiveness, including analysis of MHC protein content and activity, is now warranted.
Elevated myocardial PP2A levels have also been shown to mediate an increase in myofilament Ca2+ sensitivity. Dephosphorylation of cardiac troponin I by PP2A relieves inhibition of myosin ATPase activity and slows Ca2+ dissociation from troponin C (21, 42). Fructose-induced upregulation of PP2A subunits A and C in the present study may play a role in maintaining cardiomyocyte contractile performance despite marked suppression of Ca2+ cycling. PP2A activation may involve p21-activated kinase 1 regulated by Ras-related small G proteins (21, 22), but this possibility has not been explored in this study. NHE-mediated modulation of myofilament Ca2+ sensitivity (20) might also be involved and was investigated, since this transporter has been shown to be upregulated in rodents with genetically induced insulin resistance (13). No change in NHE-1 expression was detected. This finding does not preclude a role for pH modulation, since even without NHE1 expression change there may be altered Na+/H+ exchange activity. Expression and/or activity shifts in other pH regulatory transporters could be considered.
The low Ca2+ "operational state," an adaptive phenotype vulnerable to challenge?
The capacity of myocytes from fructose-fed mice to maintain contractile performance in the context of significant reduction in operational (systolic and diastolic) Ca2+ levels is striking. Because net contractility is maintained (equivalent twitch amplitude and maximum rate of shortening), the increase in Ca2+ responsiveness appears to offset the decreased Ca2+ availability. This finding is suggestive of a subcellular compartmentation process that may selectively direct energy intermediates to support myofilament ATPase activity in preference to SERCA2 activity. In the insulin-resistant state, while glucose uptake would be expected to be diminished, a partially augmented fructose supply may be targeted to service myofilament energy demand. Elevated ROS levels in conjunction with increased Ca2+ levels are known promoters of programmed cell death (4, 6); thus, it could be speculated that this low Ca2+ adaptive strategy protects myocyte viability in a high-stress state. We have previously shown in this model of fructose feeding that autophagy induction is upregulated (35) and identified this mode of cell death as a potential mechanism responsible for myocyte attrition and fibrosis infiltration. The longevity and robustness of such an adaptive strategy may be limited. As a relatively short-term contingency, the low Ca2+ operational state may be effective, but over the longer term and when additional loading or an inotropic challenge presents, contractile reserve may be inadequate. Indeed, a previously reported finding that fructose-fed mice exhibit more significant deterioration of cardiac function in response to transthoracic aortic constriction is consistent with this proposition (10). The adaptive strategy of increasing responsiveness to Ca2+ may be an effective short-term expediency with long-term detriment.
In conclusion, this investigation provides the first evidence that high dietary fructose induces profound disturbance of cardiomyocyte Ca2+ handling and responsiveness. We provide the first evidence that the fructose-specific GLUT5 transporter is expressed in murine cardiomyocytes. The findings from this study provide important mechanistic insight into the pathogenesis of insulin-resistant cardiomyopathy and suggest that myocyte Ca2+-handling abnormalities occur at an early disease stage, with recruitment of compensatory molecular shifts to preserve contractile function. The progression of this early adaptive short-term response to longer-term functional maladaptation requires further investigation, and extended longitudinal studies to map the time course of transition beyond adaptation/compensation are necessary. The potential clinical importance of these findings is that significant underlying cellular excitation-contraction coupling disturbance may occur before cardiac functional impact is observable in vivo in the insulin-resistant state associated with high fructose intake. This work identifies substrate for development of treatment strategies directed to molecular targets for effective intervention before disease progression to advanced diabetic cardiomyopathy.
The authors acknowledge funding support from the Diabetes Australia Research Trust and the National Heart Foundation of Australia. R. H. Ritchie is supported by a National Health and Medical Research Council of Australia Senior Research Fellowship.
No conflicts of interest are declared by the authors.
Valuable discussion with A. J. Davidoff during study development is acknowledged.
- Copyright © 2012 the American Physiological Society


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Today's Funny Story!
Stephen and I went to the 12:10 showing of X-Men Apocalypse at the Jamaica Multiplex theater located in Jamaica, Queens, New York.
We got into the movie for only $20 bucks.
Me as a Senior and Stephen as my child!!
All by showing my AARP card! LOL!!
Let's see now! Stephen just turned 55 earlier this month and I turned 57 back in February. Hmmm… That means I was two years old when I had my brother!! Ha!! Ha!!
X-Men Apocalypse Movie Review
This was a great movie. Initially the movie starts out in Egypt and even though you do see some Black or Brown skinned actors playing those roles it would have made me happier to see more people of color especially Black Women. In 3600 B.C.E. I thought there would have been any white people in Egypt. Directors and Producers need to acknowledge that Egypt is located in and part of Africa and Nubians ruled Ancient Egypt.
The directors take the audience back in time to explain some of the X-Men Mutant origins. All the cast are newer and younger actors (20 somethings) except Wolverine who is played by the same actor as in the previous movies but only has a small short role in this film. The movie also tells how the character Storm evolved from a petty thief who was initially on the dark side and how she discovered the truth transferring her allegiance to the good guys.
Without giving any spoilers a Woman mutant defeats the evil being and saves humanity. Excellent story-line and plot. Plenty of action.
Captain America | Civil War
Yesterday Stephen and I went to see Captain America | Civil War. Another enjoyable action filled movie. Stephen really enjoyed this movie and my personal favorite character is the Black Panther. Love him!! Next year Black Panther is supposed to get his own feature film I would really Love to see his role expanded. In fact I'd Love to see any Black Super Hero Male or Female role's expanded and pushed to the forefront since one sees very few African or African-American Super-Heroes and even if you do see them they always see to be the loyal buddy or side kick to the white super hero. Time for Super Heroes of African Descent to Rise to the Top where we Belong!!
Stephen and I both highly recommend both movies.


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Thanks, mouser, but will it boot faster? What are the advantages?
What *is* better about having two partitions from my experience:1. You can have the windows swap drive on a different drive than windows. This does increase performance.2. If you use one drive for the OS and software, and one for data, it's easier to wipe and reimage the drive.3. One drive for data and one drive for programs makes the program drive fragment less quickly.
And as far as the other point, I mean install the OS and applications to one partition, and store the data on the other partition. The only apps I store on my separate partition are ones that are portable...
I don't think he's suggesting that one install the OS on one partition and apps on another? I've seen this mentioned elsewhere and, like you, have never understood the point, beyond a possible benefit to be derived from having a very small windows partition that would be good for... what?
Actually, I do notice a difference even if the swap file is on a different partition, rather than a different drive. I think it has something to do with fragmentation, since the partitions fragment separately.
moved all of my internet settings ... onto the data partition.
1. Should the swap file go in it's own partition on the second drive?2. Should I think about putting my data in a partition on the second drive instead of the first? If I do that, can I still call the data partition "D:" or will the drive letters only go in order (eg C: and D: on the first drive, E: and F: on the second)?3. If I don't get the partitioning right the first time, any recommendations on a good, inexpensive partition manager utility?
I used that [sorry! EDIT: Parted Magic] for the partitioningwith the help of this tutorialit was very easy
By the way if you want to put all the temp files with PageFile.sys in the first partition on drive 2 I suggest you use a fixed size page file.
Note it is also worth keeping a page file on C: of at least 64Mb - that way if you get BSODS in the future the errors will be logged in the system event logs. If you don't have that small page file available Windows can't save Crash Dumps at all and there will be no error messages in the logs to help with trouble shooting. Again make it fixed size.Once you have set up your system use something like Perfect Disk to do a boot time defrag so that your C: and page file drives are optimized.
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I LOVE soup and it's one of our menu staples during the cold winter months. Add in some crusty bread and a green salad and I'm in heaven! Soup is simple to fix and loaded with nutritious possibilities. Sometimes, my meat-eating crew wants something more substantial than broth with a few other things in it, though. Silly goofs! 🙂 So my little experiment to take a traditional soup and make it more of a stew was born out of a desire to have all the wonderful flavors of soup in a hearty, stick to your ribs dish. It still has flavorful broth, but the "few other things in it" are the stars of the show. Turns out, it's stupendously delicious! Plus, now I've discovered a new dish that is perfect for potlucks and family gatherings!
The thing to remember about this recipe is that it makes a large batch, enough to feed 10 or 12 people, generously. Cut it in half, if you're just making it for a weeknight supper. Also, the leftovers stored very well, however, all the broth was absorbed by the pasta as it sat in the fridge overnight. To reheat it the next day, we had to add some beef broth to our bowls, before we covered them and popped them in the microwave. This tells me that this is not a dish that would freeze well, so I wanted to give you a heads up. It is flavorful PERFECTION, however, steaming hot from the stew pot! I garnished it with a little grated Parmesan cheese and more chopped fresh spinach. Even the grandkids gobbled it up!
So, grab your apron, slice some French bread, toss a quick salad and let's make an easy dish your family will love — Beefy Pasta Fagioli Stew with Spinach. Enjoy!
- 2 lbs ground beef
- 2 teaspoons high quality sea salt
- 2 teaspoons ground black pepper
- 2 Tablespoons fresh garlic, minced
- 1 large red onion, minced
- 2 Tablespoons dried oregano
- ¼ cup dried basil
- ¼ cup dried parsley
- 3 (14.5 oz) cans petite diced tomatoes, undrained
- 1 (8 oz) can tomato sauce
- 2 (14.5 oz) cans cannelini beans, drained
- 5 cups beef stock
- 1 lb small pasta (I used rings, but shells or elbows would work, too.)
- 2½ cups fresh spinach, chopped fine
- optional: grated Parmesan for garnish
- Cook and drain pasta according to package directions. Set aside.
- Brown the ground beef in a large stock pot, with the salt and pepper. When it is completely browned, drain off any fat and place the beef back in the stock pot.
- Taste the beef and check the seasoning, now. This will be your last opportunity to make sure the beef has good flavor in your stew, so add salt and pepper, to taste, if necessary.
- Add the onion, garlic, basil, parsley, oregano, tomatoes, tomato stock and beef broth to the stew pot. (If you don't have beef stock, on hand, Knorr Beef Stock concentrate is REALLY good. I love it!) Allow to come to a boil and then reduce to a simmer. Simmer for 30 - 45 minutes, to meld all the beefy, tomatoey, herb flavors.
- Add the drained beans and pasta to the stock pot and heat just longenough for the beans and pasta to be heated.
- Chop fresh spinach until it is in very thin ribbons or small pieces. Place 2 cups of the spinach into the stock pot and save the other ½ cup for garnish.
- Sprinkle with grated Parmesan and chopped, fresh spinach as garnish. Serve with a tossed salad and warm bread.
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If you're searching the web for information about Dover accident claim solicitors, it's probably because you've recently been involved in an incident that wasn't your fault, and you're eager to discover whether you could be entitled to receive a cash sum.
You will of course want to do everything that you can to ensure that you get what you deserve. Here, we discuss what you can do to maximise your chances of success.
Collect together any evidence that you might have
If you have evidence that supports your case, this is great news for you and your solicitor, and it could make a big difference to the overall outcome. Take a little while to think about what you could have access to. This could include photographs that you took at the scene with your mobile phone, receipts for medications, eyewitness testimonials, and so on.
If you don't have any of these things though, you shouldn't panic. You still might be able to claim. Speak with a legal professional for more tailored advice regarding your options.
Consider other aspects of your recovery
It's understandable if you've been spending a lot of time recently thinking about your claim for compensation. You probably have many things that you need to pay for in the near future, and this can cause a lot of stress and worry.
However, it's important that you look at the wider picture. You'll need to make sure that you look after your health and well-being and there will be other tasks that need your attention, like liaising with your employer about any time off work that you might need to take. Make a list of everything that needs to be taken care of, and create a plan so you'll get everything covered in a timely manner.
Use the services of Accident Advice Helpline
If you're looking for Dover accident claim solicitors, choosing Accident Advice Helpline would be a very wise decision.
Although we don't have access to a local firm of Dover accident claim solicitors we can still help you. We have over a decade of experience in the field of personal injury claims and we're currently one of the largest firms operating in the UK. We'll give you the type of support that you really need right now, and you can get started straightaway.
Pick up the phone and call 0800 689 0500 from a landline, or 0333 500 0993 from a mobile. This is your opportunity to speak with a friendly and highly knowledgeable adviser, without any kind of obligation. Alternatively, take the 30-Second Test online and find out how much compensation you could stand to receive.
Date Published: 13th October 2014
Author: David Brown


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The Biochemistry and Cell Biology (BCB) Master of Science Program
The Department of Biochemistry and Cell Biology offers a graduate program for the Master of Science degree. This ~1.5 year MS program is designed to prepare students for careers in research, teaching, biotechnology, or further advanced studies in health and life sciences. Our pool of faculty represents diverse research interests spanning biochemistry, genetics, cell, molecular, and structural biology. In the five years since its inception in 2010, 51 students have completed the MS in Science degree. Of these, 21 have gone on to Ph.D programs at excellent institutions including Johns Hopkins, the University of Indiana, Stony Brook, Cornell and New York University. Four students are in medical/dental/vet school, including Harvard Medical school and Columbia Dental school. Eight students are working as laboratory technicians at places such as Stony Brook University, Cold Spring Harbor, Rockefeller University and Washington University at St. Louis. Two students have science related jobs and one student is a patent lawyer for biological properties.
Program of Study
Students will be exposed to biochemistry and molecular biology related research activities, including theory and practice culminating with the MS degree. Core concepts and skills are taught through a series of required core courses, with the remaining coursework consisting of advanced electives and special topics courses selected in consultation with the student's advisory committee. A total of at least 30 graduate credits with a cumulative GPA of 3.0 or greater are required for the MS degree. Of this, 24 credits must be earned in core courses in biochemistry, cellular biology, and molecular genetics as well as courses aimed at exposing students to laboratory research, literature-based research, and advanced methods in biochemistry and cell biology. The remaining 6 credits may be selected from elective courses, special seminar courses, and courses in experimental design, data analysis and laboratory techniques.
Flexibility exists to suit individual student needs and career ambitions. Both research-based and literature-based thesis options are available, and can be completed by full-time students in three semesters. Part-time options are available, although it is expected that all students will complete the degree within a three-year period. All students are required to complete a one semester 4 credit research practicum, in which students will be introduced to modern biochemical and cell biological research techniques through participation in ongoing research in the laboratory of a Biochemistry and Cell Biology or associated faculty member. For the MS degree, at least 2 additional credits of research performed in a laboratory or on critical evaluation of current literature are also required and these studies will form the basis of a written and orally defended MS.
Your primary advisor for the first year will be the Director of the Program. The Director will meet with you prior to the initial registration for the purposes of planning specific course requirements and helping you decide on laboratory in which to complete your research practicum. The Director will meet with you during each semester to monitor your progress and plan the remaining curriculum.
How to Apply
The Graduate School (www.grad.sunysb.edu) requires on-line application submission, including letters of recommendation. At The Graduate School website you will find an Admissions link to the on-line Application form.
Applications are considered year-round, but all prospective MS students (international and USA) must apply by April 15 for admission to start in the following Fall quarter.
Admission Requirements
Most students accepted into the BCB MS program have BS or BA degree in a life science related field, with an average of B or better in their undergraduate course work. Research experience in the life sciences is not required but will be considered as a positive indicator that may mitigate a deficiency in the academic record. The Graduate Record Examination (GRE) is not required for admission, although a strong performance on this exam can be a positive indicator.
Pre-requisites: Mathematics through one year of calculus, chemistry (including organic chemistry and laboratory), general physics, and one year of biology (including laboratory). It is highly recommended that students will have taken two semesters of biochemistry, and one semester each of genetics, cell biology, physical chemistry, and English composition. Students accepted into the program without a pre-requisite may be asked to take the appropriate upper level undergraduate course prior to undertaking specific graduate level courses.
Personal Statement: What would you consider your special qualifications to be? What do you propose to do with your advanced degree, professionally? Discuss briefly your experience in biochemistry and cell biology outside the classroom.
Letter of recommendation: Three letters of recommendation from people who can evaluate the applicant's potential for graduate work and independent research.
International Students: A proficiency in the English language is required. If your native or primary language is not English, you must take an English proficiency test. To be considered for admission, an applicant must present an acceptable score on the TOEFL or IELTS test. IELTS: Overall score of 6.5 with no subsection below 6. TOEFL: Paper-based test: 550; computer based test: 213; or Internet-based test: 90. Under special circumstances, lower scores may be considered.
Core Curriculum (24 credits):
- MCB 503 Molecular Genetics (Fall, 3 credits)
- MCB 520 Graduate Biochemistry I (Fall, 3 credits)
- MCB 656 Cell Biology (Spring, 4 credits)
- BCB 551 Introduction to Research in Biochemistry and Cell Biology, Integrity in Science (Fall, 2 credits)
- BCB 552 Advanced Laboratory Methods in Biochemistry and Cell Biology (Fall, 3 credits)
- BCB 559 MS Research Practicum in Biochemistry and Cell Biology (Fall, Spring & Summer, 0-4 credits)
- BCB 599 MS Thesis in Biochemistry and Cell Biology (Fall, Spring & Summer, 0 – 6 credits)
- MCB 601 Colloquium in Molecular and Cellular Biology (Fall, 1 credit)
- MCB 602 Colloquium in Molecular and Cellular Biology (Spring, 1 credit)
- MCB 601 or 602 Colloquium in Molecular and Cellular Biology (1 credit, may be repeated for elective)
- BCB 559 MS Research Practicum in Biochemistry and Cell Biology (Fall or Spring, may be repeated for elective, 4 credits)
- BIO 558 Biological Basis of Human Evolution and Behavior (Fall, Spring & Summer)
(Fall only)
- BME 501 Engineering Principles in Cell, Tissue, and Organ Systems (3 credits)
- BME 503 Cell and Molecular Imaging (3 credits)
- BME 572 Biomolecular Analysis (3 credits)
- BME 606 Drug Gene Delivery (Fall alternate years, 3 credits)
- BSB 515 Computational Methods in Biochemistry and Structural Biology (1 credit)
- CHE 535 Introduction to Computational Structural Biology and Drug Design (0-3 credits)
- CHE 541 Biomolecular Structure and Analysis (3 credits)
- HBP 533 Immunology (3 credits)
- HBY 530 Cellular Physiology and Biophysics ( 4 credits)
- MCB 517 Membrane Biochemistry (1 credit)
- MCB 529 Organelle Development (Fall alternate years, 3 credits)
- MCB 657 Principles of Development (3 credits)
(Spring only)
- BEE 552 Biometry (3 credits)
- BGE 510 Graduate Genetics (3 credits)
- BME 509 Fundamentals of the Bioscience Industry (3 credits)
- BSB 512 Introduction to Structural Biology (2 credits)
- BSB 580 Advanced Structural Biology (1 credit)
- CHE 536 Molecular Modeling of Biological Molecules (0-3 credits)
- CHE 542 Chemical Biology (3 credits)
- HBM 522 Biology of Cancer ( 2 credits)
- HBP 531 General Pathology (3 credits)
- HBY 565 Mathematical Models of Physiological and Biophysical Systems (3 credits)
CHE 559/AMS 537 - Biological Dynamics & NetworksHBH 550 Statistics in Life Sciences
- HBH 550 Statistics in Life Sciences
(Summer and intermittent electives)
- AMS 533 Numerical Methods and Algorithms in Computational Biology (3 credits)
- AMS 537 Dynamic Models of Gene Regulation and Biological Pattern Formation (3 credits)
SAMPLE PROGRAM OF STUDY – LITERATURE-BASED THESIS OPTION (30 Credits)
The literature-based thesis option requires 30 credits comprised of 24 credits in core courses, including 4 credits of MS Research practicum, 2 credits of MS Thesis in Biochemistry and Cell Biology, and 6 elective credits. This option requires completion of a written, literature-based project. The following is a suggested plan of study for students with two full-time semesters at the G1 level (12 credits per semester) and a third and final full-time semester at the G2 level (6-9 credits).
SAMPLE PROGRAM OF STUDY – RESEARCH-BASED THESIS OPTION (30 Credits)
The research-based thesis option requires 30 credits comprised of 24 credits in core courses, at least 2 credits of MS Thesis in Biochemistry and Cell Biology in addition to the Research Practicum course included in the core curriculum, and 6 elective credits. The following is a suggested plan of study for students with two full-time semesters at the G1 level (12 credits per semester) and a third and final full-time semester at the G2 level (6-9 credits). The thesis option requires an MS thesis on research conducted in the laboratory of Biochemistry and Cell Biology faculty, in the research laboratories of faculty from other Departments at Stony Brook and at Brookhaven National Laboratory, or through research internships under the guidance of approved mentors at local biotechnology firms.
|Fall I
|MCB 520 Graduate Biochemistry
|BCB 551 Introduction to Research in Biochemistry and Cell Biology
|BCB 552 Advanced Laboratory Methods in Biochemistry and Cell Biology
|MCB 601 Colloquium in Molecular and Cellular Biology
|Elective (e.g. BME 503 Cell and Molecular Imaging (3 credits), BIO 558 Biological Basis of Human Evolution and Behavior), or combination of 1 credit electives such as BSB 515 Computational Methods in Biochemistry and Structural Biology, MCB 517 Membrane Biochemistry)
|Spring I
|MCB 656 Cell Biology
|BCB 559 MS Research Practicum in Biochemistry and Cell Biology
|MCB 602 Colloquium in Molecular and Cellular Biology
|Elective (e.g., and BSB 512 Introduction to Structural Biology)
|Fall II
|MCB 503 Molecular Genetics
|BCB 599 MS Thesis in Biochemistry and Cell Biology
|MCB 601 Colloquium in Molecular and Cellular Biology
|Total 1, 2
1. Note G2 international students must enroll for 9 credits in to maintain full-time student status for immigration purposes.
2. G2 students employed in a Stony Brook on-campus job must enroll for 9 credits to maintain full-time student status.
Contact Information
|Neta Dean
Program Director
310 Life Sciences Building
Stony Brook, NY 11794-5215
Phone: 631-632-9309
Fax: 631-632-8575
|Pamela Wolfskill
Administrative Specialist & BCB MS Graduate Program Coordinator
Stony Brook University
450 Life Sciences Building
Stony Brook, NY 11794-5215
Email: email@example.com
Phone: 631-632-8585
Department of Biochemistry and Cell Biology
|Michael Airola
|Structural biology of lipid modifying enzymes
|Paul M. Bingham
|Genetic control of development and gene expression in animals
|Deborah Brown
|Cholesterol/sphingolipid-rich domains in membrane signaling
|Vitaly Citovsky
|Nuclear targeting and intercellular communication in plants
|Neta Dean
|Glycosylation; fungal pathogenesis
|Dale G. Deutsch
|Marijuana; molecular neurobiology of anandamide
|French, Jarrod B.
|Structure, function and mechanism of proteins and protein complexes involved in human nucleotide metabolism.
|J. Peter Gergen
|Gene expression and development in Drosophila
|Steven Glynn
|Structure and mechanism of protein-unfolding machines in mitochondria
|Hannun, Yusuf A
|Bioactive lipids in cancer pathogenesis and therapeutics.
|Bernadette C. Holdener
|Genetic regulation of early mammalian development
|Nancy Hollingsworth
|Meiotic synapsis, recombination, and segregation in yeast
|Martin Kaczocha
|Role of fatty acid binding proteins in pain, inflammation, and related pathophysiologies: Endocannabinoid pharmacology and development of novel therapeutics
|Wali Karzai
|Structure and function of RNA-binding proteins and biochemical studies of the SmpB•tmRNA quality control system
|Levy, Sasha
|Evolutionary dynamics, network dynamics, yeast genomics, high-throughput technology development
|Erwin London
|Membrane protein structure/translocation/folding
|Ed Luk
|Chromosome biology and genome regulation
|Harvard Lyman
|Photocontrol of chloroplast development
|Benjamin Martin
|Stem cell maintenance and differentiation, Developmental mechanisms of cancer pathogenesis
|M. Mahmood Hussain
|Regulation of lipid metabolism and atherosclerosis by micro RNAs and circadian rhytms
|David Q. Matus
|Evolutionary, cell and developmental biological approaches to studying nematode uterine-vuval attachment and morphogenesis
|Aaron Neiman
|Vesicle trafficking and membrane/cytoskeletal interactions
|Sheppard, Keith
|Director of Science Education, Associate Professor, Three areas of science education - all with the fundamental aim of improving the teaching and learning of science at every level of education.
|Sanford Simon
|Extracellular degradation by neutrophil proteases
|Steven Smith
|Structure and function of membrane proteins
|Gerald H. Thomsen
|Growth factors /signal transduction in early vertebrate development
|Lonnie Wollmuth
|Synapses that use glutamate as a neurotransmitter
Department of Chemistry
|Elizabeth Boon
|Nitric oxide signaling in bacteria.
|Isaac Carrico
|Site-specific protein labeling; glycoproteins.
|Carlos Simmerling
|Development of tools for efficient and simulation of chemical systems and using them to study the structure and dynamics of molecules involved in biological processes.
|Peter Tonge
|Spectroscopic insights into enzyme mechanisms and structure
Department of Pathology
|Adam P. Rosebrock
|Regulation of central carbon metabolism underlying cell growth and division.
|Richard R. Kew
|Leukocyte chemotaxis/inflammation
|Kenneth Shroyer
|Cancer biomarkers as diagnostic adjuncts in cervical pathology and cytopathology; cervical cancer and HPV
Department of Pharmacological Sciences
|Bogenhagen, Daniel
|Mitochondrial DNA; DNA repair
|Holly Colognato
|Extracellular matrix in the brain; roles during development and during neurodegeneration.
|Michael A. Frohman
|Early mammalian development; gene regulation
|Miguel Garcia-Diaz
|Mechanisms of mitochondrial gene expression/Mechanisms of DNA synthesis and repair
|Masaaki Moriya
|Cellular responses to DNA damage.
|Markus Seeliger
|Molecular Mechanism of Protein Kinase and Ubiquitin Ligase signaling in Cancer and Aging
|Ken-Ichi Takemaru
|Wnt Signaling in Development and Disease
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Frequently Asked Questions
When is the application deadline?
All prospective MS students (International and USA) must apply by April 15 for admission to start in the following Fall quarter (no Spring admission is available).
What research opportunities are available?
On the website (http://www.stonybrook.edu/biochem/graduate/bcb.html ) there is a link to "People", which lists the BCB MS members & their research interests. These are potential labs in which a student may be able to pursue research. Flexibility exists and students may do research in labs outside this list as long as the project falls broadly under the category of biochemistry and cell biology.
What financial assistance or scholarships are available?
Unfortunately, we currently cannot provide financial aid. There are no tuition waivers or TA lines, though there have been part time lab assistant-ships available through Stony Brooks Undergraduate Biology Program. In general, these are not sufficient to cover tuition costs.
What opportunities are available for under-represented minority students?
Loads. For example, several of our graduate students have successfully obtained NSF Bridges to Doctorate fellowships ($30,000 for two years). For more information and opportunities, see the Center for Inclusive Education web page (http://www.stonybrook.edu/commcms/cie/)
If a student has a GPA lower than 3.0, is it possible for them to be admitted into the GraduateProgram?
The Admissions Committee examines all aspects of each application, and a low GPA may be mitigated by other strengths of the application. However, this cannot be determined in advance without seeing the student's entire application.
How many BCB MS students are accepted per year?
In 2012, there were ~120 applicants and ~15 were offered admission. 14 out of the 15 accepted our offer.
Is the GRE required for admission to the BCB MS Program?
The GRE is NOT required for admission; however, a strong performance on this exam can be a positive indicator. For foreign applicants, the TOEFL is required. We do not offer "conditional" acceptance.
Can the masters program be completed in a year?
The program is designed to be completed in three (3) semesters, but it is possible to do it in two (2), with completion of the thesis over the summer. However, to do so in an accelerated manner woulddemand that you enter the program with a very strong foundation in Biochemistry & Cell Biology.
Who can I contact with general questions about the graduate program?
Contact the Graduate School. A listing of degree programs where you may find contact information is located at http://www.grad.stonybrook.edu/ (select Biochemistry & Cell Biology under the Masters program). If you are checking on the status of your application and/or materials received, log in to your Application account at https://app.applyyourself.com/?id)=sunysb-gs. You will need your pin # and password to access your information. You may also find answers to your admissions questions on the Graduate School FAQ page at http://www.grad.sunysb.edu/admissions/faq.shtml.
Here are my GPA, GRE and TOEFL scores; does this meet the program requirements?
Without seeing your entire application, we cannot tell you for certain whether or not you will be admitted. Details about the program requirements, deadlines and how to apply can be found on our webpage: http://www.stonybrook.edu/biochem/graduate/bcb.html.
What is the requirement for each part of TOEFL?
All foreign graduate students must score a minimum of 90.
Should I contact individual faculty before submitting my application?
Do not contact individual faculty before admission. There is no point because students must first apply and be admitted to the program. However, after you are admitted, we encourage you to contact faculty that you may be interested in working with.
What type of flexibility does the program have to accommodate a full time career?
The biggest potential conflict for a 9-5 job is that most of the required courses are scheduled during the day. Therefore, students that are also employed must have the job flexibility to attend these required courses. With regard to the length of the degree program, sample study programs listed on our web page are designed to be completed in three semesters, but can be stretched out up to six semesters.
I am a permanent US resident, does that mean my tuition fees will be lower than international students?
The URL that contains a current breakdown of tuition and costs for resident and out of state graduate students is: http://www.stonybrook.edu/bursar/tuition/grad.shtml
I want to re-apply to the university this year, but am unable to start a new application or edit the previous application. What do I do?
Contact ApplyYourself. There is a technical support link that you can use.
Are my GRE & TOEFL scores competitive enough for admission?
TOEFL scores may not be below 90. The Admissions Committee examines all aspects of each application, and a low GRE may be mitigated by other strengths of the application. However, this cannot be determined in advance without seeing the student's entire application.
Can a student get admission into the masters program if they've graduated with another degree?
Yes, but preference will be given to students that have not completed an MS in another Biochemistry or related field.
I would like to apply for my MS degree in BCB and I am also interested in pursuing a Ph.D. at Stony Brook (MCB, BSB or MGM). If I were to apply to the MS program for the upcoming fall and after a semester (or full year) I decide I would like to obtain my Ph.D., would that be a doable transition? Would any of the completed MS coursework be applicable/transferable towards a PhD?
Our BCB MS students take the same courses that our Ph.D. students are required to take, so all courses would be transferable. However, admission to the PhD programs is not automatic. MS students must apply and be admitted into the Ph.D. program.
How many credits do I need to keep my student status?
9 credits
What undergraduate classes should be taken to prepare a student for a BCB MS graduate course load?
Cell Biology, Genetics, and Biochemistry (I and II)
Where on campus do Masters students usually live?
Graduate housing may be available. Contact the Graduate school to apply for on campus housing.
Can the language proficiency test for International Students who have or will graduate from an English speaking institution be waived?
If an International student has received an UG degree from an English-speaking institution, or has successfully obtained a graduate degree from an English-speaking institution, the department can request a waiver. To ensure the email comes from the corresponding graduate program director, send the email and cc the graduate program director on the email correspondence. Clearly indicate what qualifies the student to be exempt from the proficiency test. The request will be reviewed and responded to via email.
Will the department offer conditional acceptance for those applicants who do not fulfill the English proficiency (TOEFL) requirement?
What if I submitted an application to the BCB MS program in the past, and want to apply again?
The Graduate School will allow an applicant to reapply to the same program within a year. However, the applicant cannot alter any portion of their application - he/she must use the one on file. If he/she chooses to update any information, a new pin and application must be created.
Do International students need to use the WES services to process their transcripts before sending them to us?
Can a student sit in on a class that they are not registered for?
Auditing a class requires prior permission from the instructor first; not all instructors allow students to audit their courses.
If I have taken equivalent graduate courses, how many grad credits can be transferred and applied towards my MS degree?
12 credits can be transferred (as per Grad School rules). Contact the Graduate school as this rule may vary from year to year.
Where can I go for more questions about graduate school?
The Career Center website has loads of information (http://career.stonybrook.edu). Once on the website, click on Students tab on top of page, then click on Graduate & Professional Schools. At the top of the page are 3 tabs, Contemplating, Exploring & Focusing and Preparing & Applying (probably most helpful). Check out the whole website though.


text:
Results 1 to 9 of 9
September 7th, 2001, 11:10 AM #1

 if (action == "image") {
var thisImage = prompt("$vars_wordlets{enter_image}", "http://");
var imageUBBCode = " [img][/img] ";
revisedMessage = currentMessage+imageUBBCode;
document.REPLIER.message.value=revisedMe ssage;
September 7th, 2001, 01:15 PM #2
- Join Date
- January 17th, 2005
- Posts
- 2,160
Is this an exam? [img]/infopop/emoticons/icon_biggrin.gif[/img]
>>revisedMe ssage
there is a space between Me & ssage
Is that it?
September 7th, 2001, 01:21 PM #3
It is the ubb code that inserts the image in the forum ... it is inserting the space by itself and I can't figure it out.
BTW ... you see it inserted the space also on that post ... (I didn't notice that b4), if it was a test .... you passed [img]/infopop/emoticons/icon_biggrin.gif[/img]
September 7th, 2001, 01:39 PM #4
- Join Date
- January 17th, 2005
- Posts
- 2,160
I've had similar problems with java code in the past.
I'm not an expert but I just noticed a double =
>>if (action == "image")
It might even be the correct format for what I know.
Another possibility is that it's variable strings may be clashing with some of the hacks you've added :confused:
Sound Like you need Johnny Suburbs

quote:
(I'm a PHP/Coldfusion/HTML/javascript/shockwave developer for a living....)

[ 09-07-2001: Message edited by: Guffy ]
September 7th, 2001, 02:52 PM #5
The double = is there on purpose. I means 'is equal to' (but you knew that), and != means 'not equal to' [img]/infopop/emoticons/icon_smile.gif[/img]
September 7th, 2001, 03:00 PM #6
@ Haiko
You consistantly have 'space' = 'space' with the exception in this line...

document.REPLIER.message.value=rev isedMessage;

I'm no programmer, but shouldn't everything be constant and there should always be a space before and after an =
Also, shouldn't your first { be on the next line?
(edited for speeling mistooks)
[ 09-07-2001: Message edited by: the fish ]
September 7th, 2001, 04:41 PM #7
As per the PM suggestion ...
Lets see .....
[NOPE :confused: ]
[ 09-07-2001: Message edited by: Haiko ]
September 7th, 2001, 06:01 PM #8
First occurence (I know about) of this bug was 09-06-2001 08:47 PM. Experienced by clicknasty in this thread.
That URL probably won't work right now, so it was in the Lounge / Desktop show off!!!
What was added to, or removed from the system around that time? If anything was added/removed, that could be the problem... Think hard... [img]/infopop/emoticons/icon_smile.gif[/img]
Whatever the problem is, it's writing 40 characters of the UBB code, adds a space, then writes the remaining code. If greater than 80 characters, you will get another space after every 40 characters of code.
[ 09-07-2001: Message edited by: the fish ]
Have variable lengths/limits been set to 40 characters? (just another idle thought [img]/infopop/emoticons/icon_biggrin.gif[/img] )
[ 09-07-2001: Message edited by: the fish ]
September 7th, 2001, 06:34 PM #9
Trouble Ticket response from POOP:

quote:
Hello Haiko:
Thank you for contacting Infopop Support. We are aware of the situation, and it will be fixed in the next version. Version 6.1 is scheduled for released, within a couple of weeks.
Jacob Tovés
Customer Service Representative
Infopop Corporation
2030 Dexter Ave. N. Suite 244
Seattle, WA 98109
Your Original Request:
---------------------------------------- --------------
The ubb code inserts a space inside the address entered of pictures and web addresses
Thank you,
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Purrfect Auto
Review for Purrfect Auto
ERNESTINE H. on 04/28/2016
"Experience with 2003 Lexus - having been serviced for several years now at Purrfect Auto. "
Every time I have had my car serviced at Purrfect Auto - it has been a perfect experience! Necessary work was explained fully and in detail. My time and any inconvenience was considered and worked around. Work was done promptly, and within estimate. - & it is still getting me where I need to go! I would recommend Purrfect Auto without reservation!
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Articles from RotoWire's fantasy archives that mention Josh Wilson's name.
September 8, 2015
Wednesday Lineup Card: You're Gonna Hear Him, Roark
July 8, 2015
Thursday Lineup Card: We Are Familia!
I bet you can't guess who is making a case as the most dominant closer in the game right now? Yep, Jeurys Familia!
July 7, 2015
Wednesday Lineup Card: Cubs Give Motte a Shot
June 2, 2015
Wednesday Lineup Card: Foltynewicz Getting Under Control
June 30, 2014
In Some Depth: Likely Movers
In this week's edition of In Some Depth, Ryan Eisner looks at the players likely to be traded by the July 31 non-waiver deadline.
May 8, 2014
Friday Lineup Card: A Sweet-Smelling Odor
The Rangers bit the bullet and called up Rougned Odor on Thursday, hoping he'll outpace the production at second base provided by veteran retreads Donnie Murphy and Josh Wilson.
April 14, 2014
In Some Depth: Senior Captain
Derek Jeter owners will likely be frustrated by the frequent rest The Captain requires during his final season.
April 13, 2014
FAAB Factor-AL: Injuries Creating Opportunities
Koji Uehara has been unavailable to pitch the last two games - Andrew Martinez suggests possible replacement options for him and Adrian Beltre, among others.
March 30, 2014
Monday Lineup Card: Sizemore Really Does Matter
AL FAAB Factor: Go Crazy for Grady?
If Grady Sizemore resides on the wire, post-draft, Andrew Martinez points out the formats in which he should be scooped up.
March 28, 2014
Spring Training Job Battles: Final Decisions
As teams near their season openers, the final cuts are being made and job battles have been decided. Brian Pelowski takes one last look around the league as spring training comes to an end.
March 25, 2014
Diamond Cuts: The Rangers' Rough Weekend
Jurickson Profar is out 10-to-12 weeks, as is Geovany Soto, and Yu Darvish is also hurting. Jeff Stotts breaks them down, as well as a few other top injuries around the league.
February 16, 2014
2014 Rangers Team Preview: Heavy Artillery In Arlington
The additions of Prince Fielder and Shin-Soo Choo in the offseason could push the Rangers over the top and to the AL West title in 2014. There are, however, some big question marks behind Yu Darvish in the rotation.
June 26, 2013
Thursday Lineup Card: A Honed Leonys
June 21, 2013
Saturday Lineup Card: A Koji Pair Of Sox
June 17, 2013
In Some Depth: Contenders' Shopping Lists
Brian Roberts' latest injury has left a massive hole at second base. It wouldn't be surprising to see the O's shop for a second baseman before the trade deadline.
June 9, 2013
FAAB Factor - NL: Zack Attack
Zack Wheeler could debut this week - Jan Levine breaks down your bid on him in this week's article.
May 26, 2013
FAAB Factor - NL: Rehabbing Outfielders
Cameron Maybin is currently on a rehab assignment and could come off the DL soon. How much should you bid on him?
May 6, 2013
In Some Depth: Flash Junior Returns
Injuries have ravaged the Dodgers' middle infield, providing Dee Gordon with another opportunity to provide speed for fantasy owners. Ryan Eisner examines middle-infield situations in flux around the league.
April 28, 2013
FAAB Factor - NL: Nolan Arenado Gets the Call
How much should you bid for Nolan Arenado now that the Rockies have called him up? Jan Levine shares his opinion.
April 21, 2013
FAAB Factor - NL: Cingrani and Rendon Debut
Tony Cingrani and Anthony Rendon made their major league debuts this week. How much should you bid on them? Jan Levine has the answer.
April 18, 2013
Transaction Analysis: The Chase Begins
Chase Headley's activation off the disabled list was one of the more signifcant transactions of the week. Check out the rest of the week's top moves.
April 16, 2013
Wednesday Lineup Card: Hill, Hanrahan Head To DL
March 31, 2013
FAAB Factor-NL: Countless Buying Opportunities
Pictured in happier (well, at least on the field) times in Tampa Bay, Carl Crawford surprised many by rehabbing his elbow enough to be ready for Opening Day.
September 29, 2011
2011 MLB Playoffs Cheatsheet: Fewer Bankrolls This Year
There are fewer clear underdogs this year, meaning it's less profitable to draft lesser players on purportedly stronger teams. Thus, someone like Miguel Cabrera doesn't necessarily get discounted.
August 7, 2011
NL FAAB Factor: Deadline Fallout
While many are now getting an opportunity following last week's trade deadline, Mike Minor is getting a look from the Braves after Jair Jurrjens' injury.
July 29, 2011
Transaction Analysis: A New Home For Beltran
July 24, 2011
NL FAAB Factor: The Wright Stuff
July 18, 2011
In Some Depth: Crazy Eddie's Electronics Version
Chipper Jones' return in a week or two will set off a chain of events on the Braves' depth chart.
July 17, 2011
NL FAAB Factor: Who's Providing the Relief?
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text:
Joel Grimes Workshops - The Master Series: HDR Backgrounds That Rock (HD)
Duration: 45m | Video: h264, yuv420p, 1280x720 30fps | Audio: aac, 44100 Hz, 2ch | 205MB
Genre: eLearning | Language: English
Version 3 is now here! Joel has put together an updated video tutorial that takes you, step by step through the exact process he uses to create his 32 bit HDR Backgrounds. Follow him as he demonstrates the camera operations, and then as he goes through processing an HDR in Adobe's new Bridge/Raw Converter 9.0.
The results are a true 32 bit file that can now be saved as a DNG Raw file. Can this be true? Yes, this is a huge leap in the evolution of HDR! Super clean tonal transitions, superb colors, with detail in the shadows and highlights. Joel then shows how you can now take those new HDR/DNG raw files, to create stitched panos and still save the image as a DNG raw file. Wow!
This 45 minute video also covers the techniques he uses to get more mega pixels out of his camera by using both Stitching and the use of Tilt Shift lenses.
Keep in mind, that there are hundreds of ways to achieve any given post processing technique and assumes the viewer has some basic knowledge of Photoshop. The objective of this video is to give you a creative tool to fulfill your vision as an artist and as with any process there are creative decisions that only you can make. This video is recorded using Photoshop CC 2014.
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text: Video News: United Kingdom Gun debate complex for schools near Columbine In the wake of the Sandy Hook massacre, one Colorado county which includes the now-infamous Columbine High School is beefing up security, with CCTV cameras on campus relayed by a central command. But gun rights advocates say that's not enough, and that the key to school safety is arming the teachers themselves. Duration: 02:03Auteur: afpenglishTags: WEB SCHOOL LIFESTYLE Columbine for debate Gun CRIME near complex Gepost: 18 februari 2013Beoordeling: 0.0Stemmen: 0]]> © DailyMotion - Monday, February 18, 2013


text:
The tulip is one of the enduring symbols of the Netherlands and Amsterdam—but it wasn't always that way. The beautiful blooms are originally from the foothills of the Himalayas and were treasured by the Ottoman sultans in Turkey. In the early 17th century, they arrived in Holland where they were first cultivated for research at the University of Leiden. But Holland's wealthy bourgeoisie adored them and the country's farmers started cultivating them in great quantities. It turned out that Holland was the perfect environment for tulip cultivation with its low-lying sandy fields where there was plenty of water and a moderate climate.
Ironically, it can be difficult to see tulips in the city of Amsterdam itself. Here are some tips.
Amsterdam Tulip Festival
The Amsterdam Tulip Festival, which runs throughout the month of April, showcases more than 400,000 colorful and occasionally rare tulips throughout the city. Some of the key locations are Artis zoo, EYE Film Museum, Hermitage Amsterdam, Hortus Botanicus, Museum Van Loon, Rijksmuseum and many public squares throughout the city.
Floating Flower Market
The Floating Flower Market or Bloemenmarkt takes place rain or shine, summer and winter on stalls located on floating barges along the canal. In springtime, tulips of all colors reign.
Keukenhof is Holland's most magnificent flower show brimming with tulips, hyacinths, daffodils, anemones, and other spring bulbs for just a few weeks each year (March 24-May 16, 2016). There are 15 kilometers of walking trails over 32 hectares.
Aalsmeer Flower Auction
Aalsmeer Flower Auction is where 19 million flowers and two million plants are sold each day via the Dutch auction system, where the price gets lower as the clock ticks down. Open to the public from Monday to Friday from 7am to 11am.
City Parks
There are numerous parks within the city limits where you can wander amongst spring flowers. The best include the huge Vondelpark, the exquisite Hortus Botanicus, and the inspired Artis zoo.
Amsterdam Tulip Museum
The Amsterdam Tulip Museum details Holland's fascination with the tulip, including a phenomenon called Tulipmania, where during the 17th century a tulip craze took hold of the country and people even sold their houses to invest in the bulbs.
And, while you won't see tulips, there will be tons more floral delights if you happen to be in Amsterdam during the weekend of June 17th. During this time, you can visit 30 of Amsterdam's secret gardens in canal houses and museums during Open Garden Days.
>>Next: The 33 Most Instagrammable Spots in the National Parks


text:
Get contact information for Hinamon Studios d.b.a. Alpha Omega Creations LLC in Charleston, WV
Hinamon Studios d.b.a. Alpha Omega Creations LLC Tags on Party Blast: Wedding, charleston, wv, West Virginia, portraits, modeling portfolio, seniors, families, babies, boudoir, children, kids, photo, photos, portrait, digital, photography, photo, photograph, photographs, photos, pets, cats, dogs, cat, dog, studio, price, mw, Photographix, PPA, Ppwv, certified, CPP