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Active Ca2+ reabsorption in the connecting tubule
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DOI: 10.1007/s00424-008-0602-6
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- Boros, S., Bindels, R.J.M. & Hoenderop, J.G.J. Pflugers Arch - Eur J Physiol (2009) 458: 99. doi:10.1007/s00424-008-0602-6
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The kidney plays a crucial role in the maintenance of the body calcium (Ca2+) balance. Ca2+ is an essential ion in all organisms and participates in a large variety of structural and functional processes. In mammals, active tubular Ca2+ reabsorption is restricted to the distal part of the nephron, i.e., the late distal convoluted (DCT2) and the connecting tubules (CNT), where approximately 10–15% of the total Ca2+ is reabsorbed. This active transcellular transport is hallmarked by the transient receptor potential vanilloid 5 (TRPV5) epithelial Ca2+ channel, regulated by an array of events, and mediated by hormones, including 1,25-dihydroxyvitamin D3, parathyroid hormone, and estrogen. Novel molecular mechanisms have been identified, such as the direct regulatory effects of klotho and tissue kallikrein on the abundance of TRPV5 at the apical membrane. The newly discovered mechanisms could provide potential pharmacological targets in the therapy of renal Ca2+ wasting. This review discusses the three basic molecular steps of active Ca2+ reabsorption in the DCT/CNT segments of the nephron, including apical entry, cytoplasmic transport, and basolateral extrusion of Ca2+. In addition, an overview of the recently identified mechanisms governing this active Ca2+ transport through the DCT2/CNT epithelial cells will be presented.
KeywordsTransepithelial Ca2+ transport TRPV5 PTH Vitamin D Klotho Calbindin
Regulation of Ca2+ transporters
Apical membrane
Basolateral membrane
Intracellular factors
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Transporter trafficking regulators
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Transporter activity regulators
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Extracellular factors
Plasma membrane retention ↑
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Na+/K+-ATPase, NCX1
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Indirectly increased activity
Morphologic characteristics of the CNT
The above discussed distal segments of the nephron exhibit distinct morphological, as well as functional features. In the superficial cortex, the DCT/CNT region is short and flows directly into the cortical collecting duct (CCD). Midcortical and juxtamedullar nephrons, on the other hand, have longer DCT/CNTs merging with other CNT segments into arcades before transitioning to the CCD [56]. DCTs consist of two short segments, DCT1 and DCT2, both comprising a uniform population of principal cells, whereas the CNT contains both principal and two types of intercalated cells [3, 16, 43, 56]. Furthermore, the principal cells in the CNT have less cell–cell contacts and mitochondria, and their apical membrane contains fewer projections than DCT cells. Unlike the polygonal-shaped CNT cells, intercalated cells appear to be round with an apical membrane densely adorned with microprojections [43, 56]. The proton secreting α-intercalated cells have extensive apical microvilli with abundant expression of the H+/K+ exchanger and vacuolar H+-ATPase and numerous subapically localized small mitochondria, whereas the bicarbonate secreting β-intercalated cells have fewer apical microvilli, and their mitochondria tend to accumulate basolaterally, where the proton pump is also located [56]. Although the ratio of α- and β-intercalated cells vary depending on the actual physiological state, α-intercalated cells are more common in the CNT.
In addition to the ubiquitously expressed Na+/K+-ATPase, the Na+/Ca2+ exchanger (NCX1) and the plasma membrane ATPase type 1b (PMCA1b) have been found along the DCT2/CNT region, whereas the apically localized thiazide-sensitive Na+/Cl− co-transporter (NCC) and the transient receptor potential melastin subtype 6 are present in the DCT (see Xi et al. in this issue). The DCT2 region also shares additional similarities with the CNT segment, as both segments express the transient receptor potential vanilloid type 5 (TRPV5) and the Ca2+-binding protein calbindin-D28K. The tight junctions in these segments are impermeable for Ca2+, and transcellular Ca2+ transport occurs against an electrochemical gradient, supporting that Ca2+ reabsorption in the DCT2/CNT is mediated by active transepithelial transport.
Transepithelial Ca2+ reabsorption
TRPV5—the apical gate
TRPV5, also known as the epithelial Ca2+ channel, is a member of the TRP channel superfamily [29]. This channel comprises large and flexible intracellular amino- and carboxyl-terminal tails flanking six transmembrane segments (TM) and an additional hydrophobic stretch between TM5 and TM6, predicted to be the pore-forming region. The amino-terminal tail contains six ankyrin repeats [19, 54] that are important structural elements for both channel assembly and protein–protein interactions [13, 19]. Furthermore, the first extracellular loop between TM1 and TM2 contains an evolutionary conserved asparagine (N358) crucial for complex-glycosylation and in turn for regulating channel activity [11, 13, 33]. The carboxyl-terminal tail harbors three potential protein kinase C (PKC) sites, which suggests an important role for phosphorylation in channel activity. Moreover, in cultured mammalian cell systems, as well as in oocytes, TRPV5 is assembled into large homotetramers in order to acquire the active conformation state [26, 33]. Facing each other, the hydrophobic stretches between TM5 and TM6 in each subunit are postulated to form the aqueous pore centered at the fourfold symmetry axis.
Detailed electrophysiological studies have compellingly demonstrated the constitutive activity of TRPV5 at low intracellular Ca2+ concentrations and physiological membrane potentials [75]. The current–voltage relationship of TRPV5 shows strong inward rectification [29, 74, 75]. Another important functional feature of TRPV5 is the high Ca2+ selectivity, making this epithelial Ca2+ channel the most Ca2+-selective member in the TRP superfamily [75]. Finally, the generation of a TRPV5 deficient mouse strain (TRPV5−/−) provided compelling evidence for the physiological function of this channel. Active Ca2+ reabsorption in DCT2 and CNT is severely impaired in these animals as TRPV5−/− mice waste approximately six- to tenfold more Ca2+ than their wild-type littermates, which is in line with the postulated gatekeeper function of TRPV5 in active Ca2+ reabsorption [31].
Shortly after the identification of TRPV5, a homologous channel, sharing 75% amino acid identity with TRPV5, was cloned from intestine and named TRPV6 [53]. Although there are some functional differences between these channels, TRPV6 exhibits the same Ca2+ selectivity and current–voltage relationship [32, 47, 78]. Moreover, this latter channel has been implicated in intestinal Ca2+ absorption. Disturbances in the Ca2+ homeostasis were also reported in mice lacking TRPV6 (TRPV6−/−) as these animals display reduced intestinal Ca2+ absorption and low bone mineral density [1]. Although it has been shown that TRPV6 is moderately expressed in adult kidney [59] and the TRPV6−/− mice have increased urinary Ca2+ excretion, the exact role of TRPV6 in the kidney is not yet fully understood.
Calbindin-D28K—the intracellular shuttle
The principal cells of the DCT2/CNT segments are continuously challenged by a substantial Ca2+ influx through TRPV5, yet the cells manage to maintain a low intracellular Ca2+ concentration ([Ca2+]i). Maintaining the free [Ca2+]i at the basal level is essential for several reasons. High levels of free Ca2+ in the cytoplasm are known to induce apoptosis and protein precipitation. In addition, Ca2+ has an essential signaling function for many processes in the cell. More importantly, an increased [Ca2+]i has been shown to inhibit the activity of TRPV5 [75]. Based on the currently available data, three different models have been postulated for transepithelial Ca2+ transfer from the apical to the basolateral membrane. The first model is based on a passive diffusion tunneling through the endoplasmatic reticulum, vesicular transport along the microtubules involving lysosomes, and finally, facilitated diffusion. According to the second model, Ca2+-transporting cells utilize lysosomes to sequester Ca2+ and facilitate its movement to the basolateral membrane [35]. The apical Ca2+ influx through TRPV5 initiates the disruption of the actin cytoskeleton and the formation of Ca2+-enriched endocytic vesicles, which are transported along the microtubules and some fuse with lysosomes [46]. In a third model, the intracellular diffusion of Ca2+ is facilitated by the vitamin D3-dependent Ca2+-binding protein, calbindin-D28K, in the principal cells of DCT2 and CNT segments [7, 20]. Together with parvalbumin, calmodulin, and troponin C, calbindins are Ca2+-binding proteins that form a family of proteins with Ca2+ affinity [15]. Calbindin-D28K has three pairs of EF-hands that are the structural basis of the high Ca2+ affinity binding capacity [6]. Moreover, in the kidney, the expression of calbindin-D28K is restricted to DCT2, CNT, and CCD regions. It has also recently been shown that calbindin-D28K translocates to the TRPV5-containing plasma membranes upon a decrease in intracellular [Ca2+] and directly associates with this channel [39]. Due to the relatively slow Ca2+-binding kinetics of calbindin-D28K, hormone-induced Ca2+ signaling can also occur independently of the transcellular Ca2+ transport rate [37]. Bound to calbindin-D28K, Ca2+ is shuttled to the basolateral membrane, where Ca2+ is discharged into the blood flow by the basolateral Ca2+ extrusion systems. Finally, some studies reported that calbindin-D28K−/− mice fed a high Ca2+ diet have impaired renal Ca2+ handling as they excrete more Ca2+ in their urine than the wild-type control littermates [60], whereas other studies did not observe a difference that is probably due to the compensatory increase of renal calbindin-D9K expression [22]. These data suggest that calbindin-D28K facilitates the intracellular diffusion of Ca2+ in DCT2 and CNT.
NCX1 and PMCA1b—the basolateral extrusion system
The energy-consuming step of transcellular Ca2+ transport lies in the Ca2+ efflux process. In this step, intracellular Ca2+ is transported across the basolateral membrane against its electrochemical gradient, and the ions are extruded back to the blood flow. Two transporters have been implicated in this mechanism, PMCA1b and NCX1. Plasma membrane ATPases are high-affinity Ca2+ efflux pumps that maintain the resting Ca2+ concentration in virtually all cells [4]. The highest Ca2+-ATPase activity in kidney was reported in the DCT segment. However, earlier studies have suggested that the capacity of this PMCA pump in CNT seems to be insufficient to keep pace with the absorptive flux of Ca2+ because it can transport only ∼30% of the total Ca2+ efflux [2, 69]. In contrast to PMCA1b, the Na+/Ca2+ exchanger has been shown to be a prerequisite for transepithelial Ca2+ transport [2, 69]. NCX1 exchanges Ca2+ and Na+ generally in a 1:3 stoichiometric ratio. Moreover, NCX1 is a widely expressed protein as it can be found in several tissues, including the heart, brain, and skeletal muscle [45]. In the kidney, the expression of NCX1 is restricted to the distal part of the nephron, particularly the CNT segment, where it predominantly localizes along the basolateral membrane [3, 28, 43] and accounts for the remaining 70% of the Ca2+ efflux [2, 69].
Regulatory mechanisms of Ca2+ transport in DCT2/CNT
The aforementioned transporters comprise the machinery transporting Ca2+ from pro-urine to the blood in the DCT2/CNT. Several factors have been shown to contribute to the regulation of the Ca2+ transporting capacity of these particular nephron segments, which can be classified into four categories: (1) the control of the overall abundance of the transporter proteins by calciotropic hormones, (2) the rate of intracellular trafficking of the plasma membrane transporters, (3) alteration of activity of the transport proteins in the membrane by intracellular factors, and finally, (4) tuning apical Ca2+ influx by extracellular (luminal) factors.
Controlling the abundance of Ca2+ transporters
Parathyroid hormone (PTH) is an essential component of the Ca2+ homeostasis. The secretion of PTH from the parathyroid gland is triggered by changes in blood Ca2+ levels sensed by the parathyroid Ca2+-sensing receptor [8]. PTH receptors have been detected in DCT2/CNT, enabling the direct control of active Ca2+ reabsorption by PTH [57].
PTH-mediated regulation of the Ca2+ transporters was studied in parathyroidectomized rats [68]. Parathyroidectomy reduced the expression of TRPV5, calbindin-D28K, and NCX1. This decline in expression of Ca2+ transporters resulted in decreased active Ca2+ reabsorption and the development of hypocalcemia [68]. After PTH supplementation, the expression of Ca2+ transporters, as well as increased plasma Ca2+ concentration were normalized in these parathyroidectomized rats. In addition, the regulation by PTH was investigated in primary cultures of rabbit CNT cells. In these Ca2+-transporting cells, PTH resulted in an elevated expression of the Ca2+ transport proteins TRPV5, calbindin-D28K, NCX1, and PMCA1b. Taken together, these results indicate that PTH stimulates renal Ca2+ handling by co-regulating the expression of the Ca2+ transport proteins [68]. In addition, experiments in these primary CNT cell cultures supported a gatekeeper role of TRPV5 since a blockade of the apical Ca2+ influx by ruthenium red prevented the PTH-induced upregulation of the other Ca2+ transporters.
Vitamin D
The vitamin D endocrine system plays a pivotal role in Ca2+ homeostasis. In the recent years, it has become clear that the active form of vitamin D (1,25-dihydroxyvitamin D3, or abbreviated 1,25(OH)2D3) is a potent regulator of the Ca2+ transport proteins. Several groups have shown transcriptional regulation of TRPV5, calbindin-D28K, and NCX1 by 1,25(OH)2D3, whereas a 1,25(OH)2D3-sensitivity for PMCA1b is not consistently reported. Studies in vitamin-D-deficient knockout models showed an impressive downregulation of renal TRPV5, calbindin-D28K, and NCX1 mRNA that could be normalized by 1,25(OH)2D3 supplementation, whereas PMCA1b was not significantly affected [27]. On the other hand, several studies indicated that PMCA1b is positively regulated by 1,25(OH)2D3 in the intestine to increase Ca2+ absorption. Northern blot analysis indicated that repletion of vitamin-D-deficient chickens with vitamin D increases PMCA mRNAs in the duodenum, jejunum, ileum, and colon [9]. Because these studies and the role of vitamin D in Ca2+ homeostasis have been reviewed extensively [29, 64, 70], detailed information is not included in this review.
Although estrogen is generally not considered as a calciotropic hormone, it is widely accepted that it plays a role in renal Ca2+ handling. In rats, estradiol has been suggested to enhance the expression of TRPV5, NCX1, PMCA1b, and calbindin-D28K [67]. In line with these observations, a recent study with aromatase deficient mice lacking the aromatase enzyme (aromatase−/−) and, therefore, estrogen deficient, also showed decreased expression of these transporters and concomitant renal Ca2+ wasting [52]. Additionally, estradiol treatment of these animals normalized the urinary Ca2+ excretion and gene expression. In agreement with these observations, increased renal Ca2+ wasting, as well as renal stone formation in women after menopause, is a well-known phenomenon [25], suggesting that estrogens may significantly contribute to the regulation of the transepithelial Ca2+ transport in the DCT2/CNT.
Controlling the intracellular trafficking
S100A10 (also known as annexin-2 light chain) is an auxiliary protein for TRPV5 [72]. With two Ca2+-insensitive EF-hands, S100A10 is predominantly present as a heterotetrameric complex with annexin-2, which has been implicated in many cellular processes, including endocytosis and exocytosis [21]. An important regulatory role has been proposed for the S100A10–annexin-2 heteromer in TRPV5 functioning [72]. The binding of annexin-2 to TRPV5 through S100A10 was shown to facilitate the translocation of TRPV5 toward the plasma membrane. This association of S100A10 and TRPV5 takes place through a short conserved peptide sequence, located in the carboxyl-terminus of TRPV5. Moreover, co-expression of S100A10, annexin-2, and TRPV5 has been observed in DCT2/CNT [72]. Taken together, these findings show that the S100A10–annexin-2 complex is a significant component for trafficking of TRPV5 toward the plasma membrane.
The small GTPase Rab11a has also been identified as a novel TRPV5- associated protein [71]. Rab11a is one of the key regulatory proteins that controls the recycling of endosomes [10, 76]. Rab11a was found to co-localize with TRPV5 in the DCT2/CNT. Here, both TRPV5 and Rab11a are present in subapical vesicular structures [71]. In addition, a direct protein–protein interaction was observed between Rab11a and TRPV5, suggesting that TRPV5 channels, present on the apical plasma membrane, recycle from the intracellular (recycling) endosomes in a Rab11-dependent manner.
Clathrin and caveolin
Van de Graaf and coworkers observed that the extraction of TRPV5 from the cell surface takes place in a constitutive clathrin-dependent manner [73]. In addition, the same authors showed that following its internalization, TRPV5 is not immediately targeted to protein degradation. Instead, by entering a Ca2+-dependent recycling pathway, TRPV5 remained stable in the subapical endosomal fraction [73]. Another recent study by Huang et al. suggested a caveolin-1-mediated internalization of TRPV5, which was inhibited by PKC [12]. Caveolin-1 is a structural component of caveolae and is crucial for the stabilization of the specialized membrane domains. Moreover, the caveolae-dependent internalization of TRPV5 was strongly inhibited by PTH-induced phosphorylation of TRPV5 via PKC, indicating that next to its genetic effect on expression, PTH also has a rapid effect on channel abundance [12]. These findings indicate that apical sorting of TRPV5 is likely to be mediated by several mechanisms that could be differentially controlled depending on physiological needs of the body.
Regulation of TRPV5 activity at the membrane
Intracellular Ca2+, Mg2+, and PIP2
Although the Ca2+ concentration in the luminal compartment of DCT2/CNT is in the 1.0–1.5 mM range, the resting [Ca2+]i in these cells is maintained around 100 nM by NCX1 and PMCA1b. TRPV5 has a high Ca2+ selectivity, and at physiological Ca2+ concentrations, its current is mainly carried by Ca2+. In human embryonic kidney (HEK293) cells heterogeneously expressing TRPV5, currents can be activated under conditions of high intracellular Ca2+ buffering by hyperpolarizing voltage steps. Earlier, Nilius et al. suggested that intracellular Ca2+ acts as a negative feedback switch regulating TRPV5 activity. The Ca2+ current through TRPV5 is inhibited by the [Ca2+]i with an IC50 of 82 nM [50]. Considering this high affinity of Ca2+-dependent channel inhibition, the presence of the co-expressed Ca2+ buffer calbindin in DCT2/CNT plays an important role to maintain TRPV5 activity. Conclusively, the [Ca2+]i itself directly regulates channel function in order to maintain optimal Ca2+ reabsorption without excessive influx of Ca2+.
Single TRPV5 channel currents in cell-attached and inside-out patches were only detected in the absence of Ca2+ and had a conductance of ∼75 pS [51]. So far, no reliable single channel measurements have been performed in the presence of extracellular Ca2+. Another interesting feature of TRPV5 is the open pore blockage by intracellular Mg2+. Currents through TRPV5 are small at physiological extracellular Mg2+ and Ca2+ concentrations, but sufficient to increase the [Ca2+]i at hyperpolarized potentials. Therefore, block by Mg2+ and decrease of the current by extracellular Ca2+ might be physiologically important to prevent Ca2+ overload of TRPV5-expressing cells [51, 75]. In addition, Huang and colleagues reported that PIP2 activates TRPV5 and that activation of the channel by PIP2 reduces the sensitivity of TRPV5 to the inhibition by the intracellular [Mg2+] [17, 42]. In this model, hydrolysis of PIP2 by receptor activation of PLC may increase the sensitivity for Mg2+ inhibition.
Another protein called 80K-H has been shown to directly interact with TRPV5 in a Ca2+-dependent manner [23]. The 80K-H protein contains two putative EF-hands and an ER-targeting signal. This TRPV5-linked protein was originally cloned as a PKC substrate and was subsequently associated with intracellular signaling [58]. Binding with Ca2+ abolished the inactivation of the two EF-hand motifs of 80K-H, and this, in turn, reduced the TRPV5-mediated Ca2+ current and increased the sensitivity of TRPV5 to the [Ca2+]i, accelerating the feedback inhibition of the channel [23]. Moreover, 80K-H also co-localizes with TRPV5 in the DCT2/CNT. Based on these findings, 80K-H has been hypothesized to act a Ca2+ sensor to regulate the activity of TRPV5 at the plasma membrane [23].
Pro-urinary factors stabilize TRPV5 in the apical membrane
Tissue kallikrein
Tissue kallikrein (TK) is a multifunctional serine protease that is primarily synthesized in the DCT2 and CNT and catalyzes the kininogen kinin conversion [55]. TK is secreted into the pro-urine, where it mediates the formation of bradykinin that binds to the type 2 bradykinin receptor (B2R) [18]. A striking effect of TK has been observed in primary rabbit CNT cells mediating transcellular Ca2+ transport [24]. Apical addition of TK or bradykinin (BK) significantly increased transcellular Ca2+ transport that was prevented by B2R antagonists, whereas basolateral application of either TK or BK had no effect [24]. This stimulatory effect of TK was mediated by the apical B2R signaling through the phospholipase C/diacylglycerol/PKC pathway, resulting in phosphorylation of TRPV5 and subsequent delay in its retrieval from the plasma membrane. Additionally, mice lacking TK (TK−/−) waste a large amount of Ca2+ without any significant alterations in plasma Ca2+, PTH, and vitamin D3 levels or any detectable changes in the expression of Ca2+ transporters in the DCT2/CNT. These observations together highlight the importance of the regulation of the TRPV5 channel abundance in the membrane by the pro-urine TK.
Urinary pH and Mg2+
The acid–base balance has long been known to affect Ca2+ homeostasis. For example, patients with chronic metabolic acidosis waste Ca2+. Pioneering micropuncture studies have shown that chronic metabolic acidosis results in Ca2+ wasting [63]. Recent advances in total reflection fluorescent microscopy analysis allowed the identification of the molecular basis underlying these in vivo observations. Exposure of TRPV5-expressing cells to an alkaline extracellular environment (pH 8.0) caused rapid recruitment of TRPV5-containing vesicles to the cell surface and a consequent increase in TRPV5 activity [40]. In the reciprocal experiment, acidic extracellular milieu (pH 6.5) induced the internalization of TRPV5-containing vesicles from the plasma membrane, resulting in a reduced channel activity [40]. The extracellular acidity clearly affected the current kinetics resulting in diminished single channel conductance as shown by Yeh et al. [77]. Binding of protons to an extracellular glutamate near the pore helix of TRPV5 at position 522 (E522) resulted in decreased channel activity, whereas substitution with a glutamine (E522→Q522) abolished the proton sensitivity. This recognized E522 as the extracellular pH sensor in TRPV5. Based on these experiments, binding of protons to the sensor has been proposed to induce a conformational change of the TRPV5 pore helix, leading to a lowered channel activity. These observations clearly point out that urinary acidification results in decreased channel activity at the apical cell membrane, as well as in a rapid retrieval of TRPV5 from the apical membrane, both of which are likely to account for the renal Ca2+ wasting in metabolic acidosis. Also, urinary Mg2+ is known to modulate urinary Ca2+ excretion, but the mechanism underlying this relationship is unknown. In a recent study by Bonny et al., it was elegantly demonstrated that an alteration in urinary Ca2+ excretion is directly proportional to the change in Mg2+ excretion and inversely proportional to the adjustment in urine pH [5]. Because TRPV5 was inhibited by Mg2+, these data are compatible with the hypothesis that urinary Mg2+ directly inhibits Ca2+ reabsorption in DCT2/CNT, which can be overruled by an alkaline luminal pH.
Klotho is a type-I (single-pass) membrane protein predominantly expressed in tissues involved in Ca2+ homeostasis, such as kidney, choroid plexus, and the parathyroid gland [34]. The ablation of klotho causes severe multiple phenotypes in klotho-deficient (klotho−/−) mice, such as short life span associated with infertility and sternly impaired Ca2+ and phosphate metabolism [38, 65]. There is a growing body of evidence that klotho controls active Ca2+ reabsorption in the DCT2/CNT segments through several mechanisms.
In kidney, klotho is exclusively expressed in DCT2/CNT, where following extracellular domain shedding, it is secreted into the circulation and the pro-urine [13]. The secreted form of klotho exerts β-glucuronidase activity [14]. More importantly, klotho was suggested to regulate the apical entry of Ca2+ in the DCT2/CNT region. The presence of extracellular klotho robustly increased the activity of TRPV5 in cultured rabbit primary CNT cells. Moreover, TRPV5-expressing HEK293 cells also showed a significant rise in channel activity after klotho treatment that was accompanied with concomitant increased plasma membrane channel abundance [14]. In addition, removal of the complete N-glycan tree by Endo-F was recently reported to result in a more pronounced increase in TRPV5 activity compared to that of observed upon klotho treatment [44]. Recently, Cha et al. suggested sialidase rather than β-glucuronidase activity for klotho, as they observed a klotho-mediated removal of terminal sialic acids from the N-glycan in TRPV5 [11]. This cleavage exposed the underlying galactose-N-acetylglucoseamine disaccharides in TRPV5, which can directly interact with membrane-bound galectin-1, causing the subsequent plasma membrane retention of TRPV5. Interestingly, treatment with PNGaseF to hydrolyze the entire N-glycan of TRPV5 mimicked the stimulatory effect of klotho, suggesting additional mechanisms besides binding to membrane galectin-1. It should be noted that Cha et al. also reported a comparable increase in TRPV5 activity upon β-glucuronidase treatment; however, this effect could be observed only at much higher (0.1–1 μM) concentrations of the enzyme, suggesting that klotho exhibits primarily sialidase activity at physiologic concentrations (∼20–200 pM) [11]. These observations confirmed the original conclusion that extracellular klotho hydrolyses oligosaccharide chains from the N-glycosylated TRPV5, causing channel retention at the membrane and a subsequent increase in TRPV5-mediated Ca2+ influx [14]. In line with these findings, microperfusion studies have shown that CNTs from klotho−/− mice fail to respond to PTH and, therefore, waste large amount of Ca2+ [66]. Interestingly, klotho was reported to interact and increase Na+/K+-ATPase activity at the plasma membrane and stimulating the Na+/Ca2+ exchange through NCX1 [34]. Taken altogether, there is compelling evidence that klotho is a novel calciotropic factor that, amongst others, can exert its stimulatory effect on TRPV5 cell surface retention from the pro-urine in the DCT2 and the CNT.
Clinical relevance
Several clinical disorders, such as chronic renal failure or diabetes, are associated with the symptoms of dysregulating body Ca2+ homeostasis. Chronic renal failure (CRF) is frequently characterized by hypocalcemia, osteoporosis, growth retardation, and secondary hyperparathyroidism. Remarkably, the phenotype of the klotho−/− mice resembles most of these characteristics [36]. Moreover, CRF patients also have greatly reduced renal klotho levels [36]. Together with the fact that klotho can regulate the activity of TRPV5 and NCX1 via Na+/K+-ATPase, the involvement of klotho in the pathogenesis of Ca2+ abnormalities in CRF may be envisaged.
Hypercalciuria and nephrolithias, disorders with a high prevalence and socio–economic burden in the Western society, are often treated with thiazide diuretics. These drugs are known to affect the Ca2+ balance by inducing hypocalciuria. Over the last decade, it was speculated that thiazide-inhibited NCC activity stimulates active Ca2+ reabsorption in the DCT/CNT. However, recent studies indicated that paracellular Ca2+ transport in the proximal tubule due to extracellular volume contraction explains the hypocalciuria during chronic thiazide treatment [48, 49]. Hypercalciuria is also an early finding in diabetes mellitus patients. Similarly, rats with experimentally induced diabetes display a significant increase in the fractional excretion of Ca2+ [41]. However, these diabetic rats showed increased mRNA and protein levels of both TRPV5 and calbindin-D28K. Additionally, insulin therapy corrected the hyperglycemia-associated hypercalciuria and abolished the upregulation of TRPV5, suggesting that the increased TRPV5 abundance in diabetic rats is due to a compensatory adaptation to an increased load of Ca2+ secondary to hyperglycemia. Although in many pathophysiological conditions the expression level of the Ca2+ transporters is out of balance, mutations in these proteins have not been discovered yet.
Concluding remarks and future perspectives
Ca2+ reabsorption in the kidney and particularly in the distal DCT2/CNT segments of the nephron is critical in the maintenance of the Ca2+ balance. Here, TRPV5 is the gatekeeper of the Ca2+ entry, and therefore, a tight control of its activity enables the organism to adjust Ca2+ reabsorption according to any demands of the body. The available experimental data summarized in this review highlights the most important mechanisms that can actually regulate active Ca2+ reabsorption. Of these, controlling the TRPV5 cell surface expression by extracellular factors in the pro-urine is a newly discovered mechanism. Klotho delays the retrieval of TRPV5 from the cell membrane by modifying the N-glycan composition, whereas the insertion of channels in the cell membrane is promoted by TK-induced phosphorylation or alkaline pH. All mechanisms result in increased TRPV5 abundance and, in turn, regulate the entry of Ca2+ at the gate. However, the canvas is far from complete. The molecular mechanism by which intracellular Ca2+ bound to calbindin-D28K is transported to the basolateral extrusion transporters NCX1 and PMCA1b is largely unknown. It could be envisaged that the local Na+ concentration may promote the release of Ca2+; however, no experimental data are available to support this theory. Therefore, the Ca2+ transfer between calbindin-D28K on one site and NCX1 and PMCA1b on the other site needs special attention. Another interesting question to be solved is the regulation of the basolateral trafficking of NCX1 and PMCA1b in the DCT2 and CNT cells. Certain players, such as the scaffold 14-3-3, phospholemman, ankyrin, or caveolin-3, have been proposed to play a role in the trafficking of the NCX transporters in neurons and cardiac cells. Nevertheless, the basolateral sorting of these transporters in the DCT2/CNT is essentially unknown. Whether there is a crosstalk between the apical Ca2+ entry and the basolateral Ca2+ extrusion regulatory apparatus is not known. The fact that klotho increases both the channel abundance of TRPV5 in the apical membrane and the activity of NCX1 at the basolateral side certainly predicts the existence of such crosstalk [14, 34]. The main question for the coming years is how all of these Ca2+ transport proteins communicate with each other in order to facilitate optimal and regulated transcellular Ca2+ reabsorption in DCT2 and CNT under conditions of disturbed Ca2+ homeostasis.
This work was financially supported in part by grants from the Dutch Kidney Foundation (C03.6017, C06.2170), the Netherlands Organization for Scientific Research (NWO-ALW 814.02.001, NWO-CW 700.55.302, ZonMw 9120.6110). J. Hoenderop is supported by an EURYI award.
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WARNING: This is an article for readers, thinkers, music/art lovers and appreciators(Some may say I'm looking to deep into this stuff, but fuck it it's the weekend I ain't got shit to do today, proud #LonelyTweeter plus I don't get high so imma discuss musical art on Nerd's site. Weird people like myself are always on there looking for the gems and out of the box discussion topics maybe people will @ me wanting me to discuss this to distract me during the week and get me through work & school struggle at least till Wednesday).
Did Kanye West Breakdown? My take on it is that West used some incredibly dope wordplay mixed with an original delivery at his impromptu performance in London's Hammersmith Apollo this past Saturday night. The message he was trying to relay to his fans from my perspective, was that he's not with the exploitation of our culture anymore, and that he's ready to protect the authenticity of his art with his soul. This is the true definition of not selling out. Do y'all listen to the rants or do y'all just skim through it? Ha.
"Creativity Fuels EVERYTHING".
Real art depicts history as it is happening. Art, whether it was hieroglyphics, sculptures, structures, poetry, or prose passed down through generations, were ways we communicated and learned about the history of the world before there were books, the internet, Wikipedia and the rumored "Illuminati".
All you conspiracy theorist can have your suspicions about the evils of the illuminati and its global dominance, but I've seen a different kind of symbolism in Kanye's rant/sermon on top of London's Mount Hammersmith's Apollo. I'll keep it simple though because "If I talk about God my blog won't get read, Huh?"
Kanye practiced brevity in the few metaphors he delivered as a form of symbolism flawlessly. The essence of poetry that hip-hop was built on, he was trying to bring back the choir by channeling his Jesus sermon on the mount last night LOL.
"Every GOOD tree produces FINE fruit, but every ROTTEN tree produces Worthless fruit."
Basically meaning if you're art is created with good intentions there is no need for you to reach out to the wolves in sheep clothing for advertisement funds, because it will be appreciated and seen as you intended it to be seen in the first place. When you chose not to notice the fangs on that weird looking sheep and compromised your authenticity for the money they promised you, that's when you have sold out.
"Remind me again why we in this shit. Since when was making music/art about getting rich?"
He's publically praying to God begging for forgiveness for producing bad fruits (meaningless music), when he was born to produce good ones (thought provoking musical art) simultaneously releasing the guilt from his conscious.
A guilty conscious is a heavy price to pay; the reason being is because that's with you even in your most peaceful state as a human, which is sleep. Dreams tell a lot homie. Nightmares tell the most truth because the truth is ugly. It's ugly in order to keep the weak from it, but inside the truth is so beautiful and freeing.
"Every niggas tryna get rich. Every rapper tryna get rich. And every rapper always rapping about fucking somebody else bitch."
The mainstream songs in this genre are mostly all about the same old redundant bullshit. The music industry is using this confused love of money formally recognized as "greed" to get artist to compromise their art; which is basically a form of selling out. What you decide to put out in this world defines you, whether it is your actions, thoughts, profession, or family life. These are all part of your image and how the jury in the sky will judge you when the time comes. You can sell that image for cheap riches (i.e. the man made paper dollar, that will depreciate in time), or you can go for that which God made such as incomparable gold. The message being to preserve your image, an artist remembered for music with cathartic qualities, and not for putting out bullshit.
It's cool to have the fan base and lane to express your art but what's the point if your strings are getting pulled telling you that you have to tweak it to get out a message that they want out, sounds like slavery to me.
West trying to remind us that we as people are trying to accomplish greatness for all the wrong reasons (i.e. wanting to get rich and fuck a fine phat ass chick), I mean that's every man's dream is it not? But why are we in this life? Isn't it to do our part as individuals, and not to follow the masses through the road most traveled? "The road to the light is the narrow path", the unoriginal are taking the obvious path because they've observed many others before them greatly benefit from the meaningless things we were brought up to idolize, by taking the easy route. We have to remember that we were born with nothing and when we die we can't bring anything with us. The only option we have is to do what we love and leave a great legacy.
"We all gonna die someday. So I'mma live my life my way."
You can only be who you are and that should be enough. You designed yourself. You have the choice to choose what you want to contribute to the world. Who cares if people don't think it's cool. Cool was unique and original before it became a commodity for at the expense of a developing lost generation.
The key to being successful is devotion to your goals along with self-sufficiency, you don't NEED anybody to put your plans in motion but yourself and the resources you have. Passion over business.
"Real niggas don't live too long in this shit!"
Now that Kanye's found his way he's asking for the strength and endurance to continue to do things his way, and not let the love of money tempt him anymore. Real niggas know u can't keep it too real in this these times. You'll either get black balled or die due to your own self destructive habits. West probably won't easily succumb to the temptations of gluttonous wealth now seeing as how his pockets are already morbidly obese and the loss his mother may have killed that appetite.
I once read "For the love of money is a root of all sorts of injurious things, and by reaching out for this love you will go astray of the faith and have stabbed themselves all over with many pains," this easier said than done because having money not everything but not having it is.
"I lost my mother fuckin momma! So I could give a fuck about your comments! I promise."
That line alludes to the fact that the only real opinion he respected was from his mom which is the same person that he would play his music for and at times when he strayed from what was pure, she would say to him "Now Kanye you know that's not you, be real to your artistic voice." Ironically she passed away too early because of the temptation to have a more attractive younger body. He's trying to remember why artists want to be artists in the first place, and the answer's not to be rich and famous.
Man makes things, but when they channel their inner God by keeping the message righteous and true to their soul those things then become art; a memory of a human ascending burned into your brain.
Real artists don't care what others think; I mean we do but fuck it if you don't get it, that's completely cool with us because we're pleased enough to put it out and its liberating that we did it our way. Artist love to say "Haha. Fuck you. I knew it would work my way". It's our life and to be completely happy you gotta live it righteously in your way.
So yes, I believe all the criticisms by people and the pain caused by the corporations having him compromise his art caused him to have one of those historically epic cut off his own ear breakdowns. In doing so he gave the world one of the greatest breakdowns of all time. ALL TIME. In a classic Superfly Louis Vuitton Don fashion. He planned this because now he knows we're in an age where you don't need corporate ran T.V. or radio to get your musical art heard. I guarantee that is a lot less painful and more conducive than going all H.A.M. Van Goh style.

subset: commoncrawl


text: NEW YORK, June 14, 2013 /PRNewswire/ -- Corvex Management LP ("Corvex") and Related Fund Management, LLC ("Related"), today issued the following statement regarding the report by Institutional Shareholder Services (ISS), a leading independent proxy advisory and corporate governance advisory firm, recommending that the shareholders of CommonWealth REIT (NYSE: CWH) vote to remove the entire board of trustees at CommonWealth. Keith Meister of Corvex and Jeff T. Blau of Related issued the following statement: "This is a monumental recommendation from a leading proxy advisory firm in that it recognizes the need for immediate, wholesale change to CommonWealth's board. We are pleased that ISS strongly supports our effort to stop the value destruction at Commonwealth and free the Company from its abysmal corporate governance practices and continued mismanagement by the Portnoys. This consent solicitation is a referendum on CommonWealth's board and management and a successful remove vote will create a clear path for shareholders to nominate truly independent and accountable trustees who are committed to the future success of CommonWealth for the long-term benefit of all shareholders. Make no mistake, our only agenda is to effect change and remove CommonWealth's trustees and we appreciate the strong and broad support of those who have already voted in favor of change at CommonWealth. The arbitration process is already well underway and we anticipate a prompt resolution on matters related to our efforts to effect change at CommonWealth. As CommonWealth itself noted, the arbitration process 'provides for an expedited process for resolving disputes.'" In its report, ISS noted that: "Votes FOR removal of all existing directors are warranted given that the dismal returns to shareholders over an extended period prior to the dissidents' arrival, the links between underperformance on key drivers of shareholder value and the inherent conflicts of interest in the external management structure the company maintains, and the current board's use of corporate governance provisions to entrench itself, in aggregate form a compelling case that change at the board level is necessary."


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QuickBooks Payments (quickbooks.intuit.com/payments/), formerly known as "QuickBooks Merchant Services" or "QBMS," is a credit card processing option included with the QuickBooks accounting software by Intuit. The backend card processing services for QuickBooks Payments are handled by Intuit Merchant Services. We have decided to review QuickBooks Payments separately because the terms and conditions of a QuickBooks Payments account are different than those offered through Intuit's traditional merchant accounts. Intuit also appears to be gradually folding its GoPayment mobile processing solution into QuickBooks Payments under the name "QuickBooks GoPayment," so merchants should be sure to clarify which product they are signing up for. QuickBooks Payments allows merchants to process credit cards via their QuickBooks accounting software, which also includes automatic bookkeeping of the transactions. Brad Smith is the CEO of Intuit, which is headquartered at 2632 Marine Way, Mountain View, California 94043.
QuickBooks Payments Products and Services
- Debit and credit card processing
- Virtual terminal
- EMV acceptance
- E-mail invoicing
- ACH processing
- Mobile phone processing
- Retail
- E-commerce
Related: Phillip's Top All-Purpose Processor Picks
Sales & Marketing
Key Points - Sales & Marketing
|Employs Independent Resellers
|Advertises Deceptive Rates
|Discloses All Important Terms
QuickBooks' credit card processing option is primarily marketed through direct email and mail marketing, online advertising, and via the QuickBooks accounting software. Intuit doesn't appear to use independent sales agents, but does have a reseller program that allows other sales organizations to market and sell its services. These third-party organizations may contract with their own independent agents, which could inflate pricing or cause changes to terms and conditions. For this reason, merchants are advised to deal directly with Intuit when setting up a QuickBooks Payments account. We are unable to find any complaints that mention nondisclosure of fees or deceptive rate quoting from QuickBooks Payments, so we'll assign the company an "A+" rating for now.
Phillip's Top E-Commerce Picks
Costs & Contract
Key Points - Costs & Contract
|Swiped Rate
|1.6% + $0.25 or 2.40% + $0.25
|Keyed-in Rate
|3.2% + $0.25 or 3.40% + $0.25
|Early Termination Fee
|PCI Compliance Fee
|Equipment Lease Terms
There is no setup cost for a QuickBooks Payments account other than purchasing the QuickBooks accounting software. Additionally, there is no service length requirement or termination fee for cancelling the QuickBooks credit card processing option. However, merchants who accept a free copy of QuickBooks in exchange for setting up a QuickBooks Payments account may be subject to a software "recovery fee" if they cancel service within 24 months of opening the account. The recovery fee is stated to be the market cost of the QuickBooks accounting software as of the date of cancellation.
QuickBooks Payments offers two separate pricing plans for merchants. The standard plan is free to use and charges 2.40% plus $0.25 per swiped transaction and 3.40% plus $0.25 per keyed transaction. The pro plan charges a monthly fee of $19.95 and offers lower rates of 1.6% plus $0.25 per swiped transaction and 3.2% plus $0.25 per transaction. Both plans charge a flat $0.50 per ACH transfer. Merchants may also be required to pay other incidental fees as well as an annual PCI Compliance fee that is based on the number of estimated transactions per year: $35 for 1-24 transactions, $50 for 25-99 transactions, or $100 for 100+ transactions. Merchants are encouraged to fully read and understand the pricing portion of the merchant application before setting up an account.
It's important to note that merchants who sign up with Intuit Merchant Services to use desktop terminals or POS systems will be subject to different terms and conditions than those offered by QuickBooks Payments. The terms through Intuit Merchant Services could include cancellation fees.
Phillip's Top Mobile Processing Picks
Complaints & Service
Key Points - Complaints & Service
|Total Online Complaints
|Live Customer Support
|Most Common Complaint
There are relatively few QuickBooks Payments negative reviews considering the popularity of the QuickBooks accounting program among small businesses in the United States. However, among the available complaints, the most common types found regard difficulty using the program and its credit card processing features (QuickBooks does require a little training if you are new to accounting programs), fund holds, account closure, failed integration with the QuickBooks point-of-sale software, and difficulty getting issues resolved with customer support. Due to the low amount of complaints, these reports appear to be mostly isolated incidents and do not indicate widespread problems.
Phillip's Top "High-Risk" Processing Picks
QuickBooks Payments does not have a dedicated Better Business Bureau report, so this portion of our review will not be factored into the service's overall rating. Intuit's main BBB report, which covers its entire suite of products and services, has an "A+" rating. The grand majority of the complaints filed with the BBB have been resolved to the customers' satisfaction.
QuickBooks Payments Bottom Line
QuickBooks Payments is a very popular credit card processing service among merchants who use the QuickBooks accounting software. Overall, the costs and fees of the service are about average for the industry; however, QuickBooks Payments has no cancellation fee, which makes it an attractive option for many merchants. The service itself has relatively few complaints, but merchants are encouraged to read and understand the terms and conditions before signing up, and to take basic QuickBooks training via a course or self-study. It appears that merchants who properly educate themselves are unlikely to experience problems.
About Phillip Parker
Hi, I'm Phillip and I'm disgusted by the state of credit card processing in the U.S. and abroad. I believe that the industry has been overrun by people who engage in fraud and deception in order to steal money from hard working business owners. I've made it my mission to expose the companies and individuals who engage in predatory marketing, pricing, and contracts, or just provide terrible service. Along with uncovering the bad guys, I've also discovered the good guys who do stand out from the status quo. CPO is a website where you will find ratings and reviews of these companies along with advice on how to save money and which service providers consider. Together we can move the industry in a positive direction. If you would like to help support my work, please checkout "Fee Sweep" my eGuide to getting the lowest possible fees when accepting card payments. If you haven't heard of "interchange" this advice will save you hundreds, even thousands, in processing fees.Schedule a Consultation with Phillip
Related: Phillip's Top All-Purpose Merchant Account Picks
All-Purpose Merchant Accounts:
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Any unauthorized copying and reproduction of the content of this page, including all meta data and computer code, is strictly prohibited. While the information in the above article is believed to be accurate as of its publish date, the author and publisher make no representation or warranties with respect to the accuracy, applicability, fitness, or completeness of the contents. The author and publisher shall in no event be held liable to any party for any direct, indirect, punitive, special, incidental or other consequential damages arising directly or indirectly from any use of this material, which is provided "as is," and without warranties. Any and all use of trade names and/or marks are for identification purposes only and shall not be construed as a claim of affiliation, or otherwise, with CardPaymentOptions.com, Inc. ("CPO") in any form. The sole purpose of the material presented herein is to alert, educate, and inform readers. It is not intended as legal or financial advice.


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Enjoy the Tranquility of Woodstock's Oldest Bed & Breakfast
Twin Gables of Woodstock is your doorway to this "Colony of the Arts". With Victorian charm and period furnishings, Twin Gables gives you the perfect location to explore Woodstock's world renown art, music and literature. Established in 1926, it is the oldest Bed&Breakfast in Woodstock, Take a dip in one of the local watering holes, many located within walking distance of this rustic B& B. Explore the great outdoors with the Catskill Mountains providing picturesque views, or visit the nearby Woodstock Farm Animal Sanctuary for a fun afternoon. Make your next trip to the East Coast a truly memorable experience by staying at Twin Gables of Woodstock!
- Wifi
- Restaurant Onsite
- Pets Allowed
- Property Size 10 units
- Conference Facility
- Kids Allowed
- Nearby City Woodstock
- Nearby Water Mill Stream
- Open Dates All Year
Established in 1926, Twin Gables of Woodstock is the oldest Bed & Breakfast in the Woodstock area. The Victorian house features period furniture and finishes that transport travelers to a time when this area was flourishing into Utopian artists' community it has become today.
The Catskill Mountains provide breathtaking views that will make your visit to Twin Gables of Woodstock unforgettable. Enjoy downhill skiing or snowboarding at local mountain destinations such as Hunter, Belleayre or Windham, located just a short drive away. For young children, Woodstock features Sled Hill, the perfect winter destination for kids.
Twin Gables of Woodstock provides the perfect four-season hideaway with outdoor attractions for every season. Conquer the Catskill Mountains by exploring the many hiking and biking trails that traverse the rocky wilderness. When the snow starts to fall, these same mountains turn into a skiing and sledding paradise. Sled Hill, an aptly named sledding hill, sits in the village of Woodstock.
The peaceful tranquility of Twin Gables of Woodstock provides the perfect rustic setting to rekindle your romance. Enjoy the artistic culture of the Woodstock area, and bask in the beauty of the Catskill Mountains. Without the distractions of television or radio in any of the rooms at Twin Gables, focus on the intimate details of relaxing weekend with your special someone.
Additional Information
- Biking/Bicycling
- Cross Country Skiing
- Downhill Skiing/Snowboarding
- Freshwater Fishing
- Hiking
- Wildlife & Nature
- Photography
- Shopping
- Sightseeing
- Swimming
Languages Spoken
- English
Nearest Airports
- Dutchess County Airport (POU) / 31.1 miles
- Stewart International Airport (SWF) / 37.1 miles
- Albany International Airport (ALB) / 51.5 miles
* Not all airports listed here may be open to public use, or service commercial flights
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Shot of the Day: March 10, 2012 from Trump International
In the third round of the Puerto Rico Open presented by seepuertorico.com, Ryo Ishikawa holes a birdie chip shot on the par-5 15th hole.
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Moving a Magento e-commerce site to a new domain name by copying an existing installation can be a confusing task if you don't know where to begin. If you find yourself in need of doing this, use this guide to save you some headaches.
Step 1 - Setup the new domain
It might go without saying, but the first step is to configure the new domain's web hosting with the required Magento dependencies, usually just the LAMP stack. Verify that you can load up a PHP page on the new domain before going any further just to take another variable out of the equation.
Step 2 - Export/Import the MySql Database
The next step is to export the MySql database from the existing Magento site and use the resulting file to import into the new Magento site. Because a Magento database can be fairly large, I recommend using the command line to perform a mysqldump operation like so:
mysqldump -u [username] -p [database_name] > [dumpfilename.sql]
Once you have your .sql file, copy it over to the new domain and import the file into your new MySql database.
mysql -u [username] -p [database_name] < [dumpfilename.sql]
Other methods for importing and exporting a MySql database are also available.
Step 3 - Copy the existing installation directory to the new domain
The reason you're going through all of this trouble is to start a new site using an existing site as a baseline. For this reason, you want to copy/paste the entire installation directory from the existing install into the new domain web root folder. Usually you'll want to compress the directory before you move it to speed things along if you're going between servers.
tar zcf existingMagento.tar.gz /path/to/webroot/*
Then after you move the compressed archive, expand the archive into your new webroot.
tar zxf existingMagento.tar.gz
Now that the archive has been expanded into your new webroot, you'll probably need to adjust the ownership of the files - a commonly overlooked step.
chown myusername:mygroupname /path/to/webroot -R
Step 4 - Adjust the Magento configuration
You'll now need to update the Magento configuration for the new site. This involves editing the config file to connect to the new database location and editing the database directly to set the proper domain name.
To adjust the config file, edit the contents of path/to/magento/app/etc/local.xml so that the database connection information matches your new parameters:
Next, open up phpMyAdmin or another MySql management tool and connect to your new database. Open the table named "core_config_data" and edit the values for "web/unsecure/base_url" and "web/secure/base_url" to match your new domain name.
Step 5 - Clear the Cache/Sessions
The final step is to clear out the cache and session files that may be present from the old installation. To do this, navigate to path/to/magento/var/cache and delete everything from the folder:
rm -rf path/to/magento/var/cache/*
Now, do the same for the session folder at path/to/magento/var/session
rm -rf path/to/magento/var/session/*
At this point you should be able to load up your new Magento installation on the new domain without having to start from scratch.
Read more of Matthew Mombrea's ByteStream blog and follow Matt on Twitter (@mombrea) and Google+. For the latest IT news, analysis and how-tos, follow ITworld on Twitter and Facebook.


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James Anthony Terry
October 30, 2012
James Anthony "Tony" Terry, age 56, of Greybull, Wyo., died Friday morning, Oct. 26, 2012, at the Washakie Medical Center in Worland, Wyo.
Memorial services will be at 10 a.m. Friday, Nov. 2, 2012, at the Fraternal Order of Eagles Aerie No. 3086 in Basin, Wyo. A memorial graveside service will follow at 10 a.m. Monday, Nov. 5, 2012, at the Knez Cemetery in Craig.
James Anthony "Tony" Terry was born Feb. 27, 1956, in Craig, the son of James Elmer and Mary Lou (Drolc) Terry. He graduated from high school in Casper, Wyo.
Tony moved to the Big Horn Basin area in 1998.
Tony met and married Elaine Jean Herman on July 22, 2000, in Greybull, Wyo.
Tony loved to decorate for the holidays. He enjoyed doing yard work and was always camping.
Tony enjoyed his last trip in September with his wife and the Eagles Aerie No. 3086. Tony was the president of the Eagles Aerie No. 3086 in Basin, Wyo., four times, and for a long time he called "BINGO" at the Eagles every Sunday.
Tony is preceded in death by his brother, Dan Terry.
Tony is survived by his loving wife, Elaine Terry, of Greybull, Wyo.; his parents, James E. and Mary Lou Terry, of Craig; his son, Josh Maxwell, of Greybull, Wyo.; his daughter and son-in-law, Tammy Maxwell-Griffis and Dan Griffis, of Hemet, Calif.; his granddaughter, Kristina Griffis, of Hemet, Calif.; his brother, David Terry, of San Francisco, Calif.; his sisters and brothers-in-law, Marcia and Johnny Steffredo, of Craig, and Marsha and Mike Scullion, of Craig; his sister-in-law, Robynn Terry, of Basin, Wyo.; and numerous nieces and nephews.
Atwood Family Funeral Directors, Inc. is in charge of arrangements.


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Students who qualify for a 504 Plan based on the Rehabilitation Act of 1973 and Americans with Disability Act are provided accommodations to ensure equal participation in the school setting. A student with a disability under this Act has a mental or physical impairment that substantially limits one or more life activities such as self-care; performing mental or physical manual tasks, walking, seeing hearing, speaking breathing, learning and working. Accommodations may include: extra time, testing in a separate location, specialized equipment, and preferential seating.
Instructional or related services for a student receiving special education services will be determined by the student's individualized education program.
A student who is unable to attend school because of pregnancy will be provided home instruction, correspondence courses, or other courses of instruction when the student's physician indicates, in writing, that she is medically unable to attend regular classroom instruction (1) before the birth of the child, and (2) for up to 3 months after the child's birth or a miscarriage.
Response to Intervention (RTI)To best meet the needs of all students, a multi-tiered system of supports is in place that includes: classroom differentiation and additional instruction in reading, math, and behavior. A detailed explanation of the Response to Intervention Process (RTI) can be found on the District's website.
Special Education


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Your Dog, Your Life
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Wildebeest creates the perfect present for new dog parents.
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Photo Comments
Hello my friends. It's been a while since my last entry and it's about time my Mom stayed in one place.We are back in Iowa after our stay in the Caribbean. One day all of a sudden there was the door on my pet carrier again and I got sooo scared because I though I have to leave my new Forever home again. Normally the carrier is where I like to nap. But there where not one, but 3 carriers sitting in the living room. I looked at Luna and I could tell she was scared too. Mom took us to the dogtor for shots and the next thing I knew I was in an airport. Mom tried to explain to us what was happening, but we were to scared to listen. Me and Luna was loaded on a trolley and then into an Airplane with a huge room full of luggage. Dagobert was able to fly in the cabin because he only weight 20 lbs, the lucky dog. The next thing I knew we were loaded on a trolley again. Where are we? I barked and barked and barked for my Mom. She must of heard me, because all of a sudden there she was. I was so happy to see her again. She let us out of our carrier to a place where it was so warm and the people all had darker skin. She took us to a wonderful house that had a swimming pool. In the background I heard this sound I never heard before. Mom told us this was the ocean. I ran to it and tasted the water. Yukkkkkkk what is this salt doing in that? There were big rocks and sand I could dig in. But wait, what is this thing that's crawling out of here? The chase was on. It tried do dig back in and I tried to dig it out. Luna and Dagobert were just standing there and wondering what was happening. Finely I caught the crab and I ate it. Not bad, it tasted a bid salty but gooooooood. From that day on we went to the ocean twice a day and I got to see many different species and I taught Luna how to go crab hunting and swimm in the ocean. Dagobert just stuck his nose up at us, strolled on the beach and taking a little dip in the ocean every now and then. I was wondering what all those shoes were doing on the beach, there was baby shoes, hiking boots, sandals, all shapes and sizes. But the funny thing on it was, there was only 1 shoe of each. What happened to it's match? If you like to know, you have to read the book my Mom is writing "Scooter and the island of the lost shoes". I'm gonna say goodbye for today. Come back and read some more of my travels.
I finally arrived at my new furever home. I have an older brother , a Westie named Dagobert "the Rocket Dog" who is 9 and a sister Luna, also a Westie who is 11 months old and real tiny. It was hard for me to move to my new family, because my foster Family in Omaha loved me sooooooo much. There I had 2 brothers named Petey and Milton. Petey was so much fun to play with, Milton is a Mommy's dog. And I loved my Foster Mom Debbie, Dad Eric and their skin kids . She works so hard for the Little White Dog Rescue in Omaha and allot of Pups found their new Furever homes because of Debbie. Thank you so much Debbie for giving me such a loving home while I was there.
Now I have to get used to my new home in Iowa. I already found my favorite place to lay, it is my Moms recliner. I met the neighbor dog, a Chesapeake Bay Retriever named Ruger and told him my opinion. On my first long walk I checked out all the Westies that live on route and I got to see the horses.
I will enter new things in my diary as I get to know the surroundings.
Copyright © I-5 Publishing, LLC. All rights reserved.
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By his knowledge shall the righteous one, my servant, make many to be accounted righteous; and he shall bear their iniquities.
He poured out his soul to death, and was numbered with the transgressors; yet he bore the sin of many, and made intercession for the transgressors. (Isa. 53:11-12)
For the love of Christ urges us on, because we are convinced that one has died for all; therefore all have died. And he died for all, that those who live might live no longer for themselves but for him who for their sake died and was raised. (2 Cor. 5:14-15)
Looking to the efficacy of the passion, we believe that the Redeemer shed his blood for the salvation of all men; but looking to the advantages, which mankind derive from its efficacy, we find, at once, that they are not extended to the whole, but to a large proportion of the human race.
With great propriety therefore, were the words, for all, omitted, because here the fruit of the passion is alone spoken of, and to the elect only did his passion bring the fruit of salvation. (p. 155)
Here, therefore, rather than at the consecration of His body, is appropriately commemorated the Passion of our Lord, by the words which shall be shed for the remission of sins. For the blood, separately consecrated, serves to place before the eyes of all, in a more forcible manner, the Passion of our Lord, His death, and the nature of His sufferings.
The additional words for you and for many, are taken, some from Matthew, some from Luke, but were joined together by the Catholic Church under the guidance of the Spirit of God (Matthew xxvi; Luke xxii). They serve to declare the fruit and the advantage of His Passion. For if we look to its value, we must confess that the Redeemer shed His blood for the salvation of all; but if we look to the fruit which mankind have received from it, we shall easily find that it pertains not to all, but to many of the human race. When, therefore, our Lord said: "For you," He meant either those who were present, or those chosen from among the Jewish people, such as were, with the exception of Judas, the disciples with whom He was speaking. When He added, "And for many", He wished to be understood to mean the remainder of the elect from among the Jews or Gentiles.
With reason, therefore, were the words for all not used, for in this place the fruits of the Passion are alone spoken of, and to the elect only did His Passion bring the fruit of salvation. And this is the purport of the Apostle when he says: Christ was offered once to exhaust the sins of many; and also of the words of our Lord in John: "I pray for them; I pray not for the world, but for them whom Thou hast given me, because they are Thine" (Hebrews ix; John xvii).


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The day after the New York Giants thrilling overtime win over the San Francisco 49ers that will send them to the SuperBowl, we've got an update on former "Giants Girl" Reby Sky and her boyfriend, Matt Hardy. Longtime wrestling photographer Bob Mulrenin recently scored an exclusive photo session with Matt Hardy and his "Giants Girl" – and had this to say about their rocky relationship:
"Matt and Reby's relationship has been the topic of a lot of discussion lately. They've been tested severely by being splashed all over the pages of TMZ, but it looks to me like their relationship is as strong as ever!"
To view Mulrenin's exclusive photo gallery, head over to Paul Heyman's HeymanHustle.com. When the Giants defeated the 49ers, Hardy tweeted:
"Wow, what a game! @RebySky is so happy that she's out of breath & shedding tears of joys. The Giants are going to the Super Bowl."
The emotional Reby simply tweeted:
"Words can't describe… #GIANTS #superbowl"
"Reby is now concentrating on her career as a professional wrestler," Mulrenin noted. "Matt's getting his legal issues addressed, and continues to train Reby, who seems to really love being in the ring!"


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Hospice of West Alabama
About Hospice of West Alabama3851 Loop Road
Tuscaloosa, AL 35404
Price & Availability: (866) 308-0477
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The Starks
House Stark is the noble house ruling The North. They trace their lineage back to the First Men, and have served as rulers of the North since long before the Andal invasion.
During the Targaryen invasion the last Stark king, Torrhen, saw the futility of combat and in an attempt to save thousands of his men knelt before the Targaryen king ending the war. He became forever known as "The King who knelt". For his wisdom he was styled Lord Paramount of the North and Warden of the same. It is a title that the Starks carry to this day.
Their seat is at Winterfell and their words are, "Winter is coming." Their sigil is a grey direwolf running across an ice-white field.
EditNotable Starks
- Eddard Stark
- Catelyn Stark
- Robb Stark
- Sansa Stark
- Arya Stark
- Bran Stark
- Rickon Stark
- Jon Snow
- Benjen Stark
EditBannermen TO HOUSE STARK
- House Bolton of the Dreadfort.
- House Cerwyn of Castle Cerwyn.
- House Flint of Widow's Watch.
- House Glover of Deepwood Motte.
- House Hornwood of Hornwood.
- House Karstark of Karhold.
- House Locke of Oldcastle.
- House Manderly of White Harbour
- House Mormont of Bear Island.
- House Reed of Greywater Watch.
- House Tallhart of Torrhen's Square.
- House Umber of the Last Hearth.
- House Cassel
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Need assistance with editing this wiki? Check out these resources:
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What Links Here
Fire and Blood | House Stark | The Wall | Theon Greyjoy | What Is Dead May Never Die | The Old Gods and the New | Septa Mordane | Maester Luwin | Religions | Moat Cailin


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Lacrosse news straight to your inbox.
Tuesday August 6th, 2013 1:01am
Early this spring we sent out a call to action for readers of Inside Lacrosse to send in their questions for the Crooked Arrows cast and crew. Via Facebook, Twitter and InsideLacrosse.com, we got a huge response.
We selected the best ones for the May issue of Inside Lacrosse Magazine. But since we didn't want to leave anyone out, here's the full list of questions and answers. Thanks to Crooked Arrows for taking the time to respond, and be sure to check out the movie when it opens nationwide on Friday, June 1.
It opened in limited release May 18 and has gotten great reviews all the way around. If you're a lacrosse fan, you absolutely need to check this movie out.
Also, be sure to listen to this podcast with producer J. Todd Harris from the week after their big opening. And check out CrookedArrows.com for more information.
Scott McConnelee: How big of an impact do you feel this film will have on a sport that is already rapidly growing?
CA: We definitely feel like we're hopping onto a moving train, but also think we're bringing more fuel for the fire. Where the movie can have the most impact on the sport's growth is introducing lacrosse to tens of thousands of young people who have never played it and will hopefully discover how great it can be and get involved.
Gary Steinberg: Besides sports, what is the difference between Crooked Arrows and The Mighty Ducks?
CA: The Mighty Ducks was definitely an inspiration for Crooked Arrows, along with other classic sports dramas like Hoosiers and comedies like The Bad News Bears. One difference is that the players in Mighty Ducks were very young — around 12 years old. Crooked Arrows features high school players — who were actually played by guys just a bit older in most cases. More importantly, The Mighty Ducks, wonderful as it was, didn't exactly showcase great hockey. Crooked Arrows lacrosse sports action, orchestrated by Sports Studio, features some very high-quality lacrosse, which should please those who play and feared we'd be doing American Pie-type lacrosse.
PK in New Jersey: What measures did you take to train the actors so they looked convincing as lacrosse players so quickly? Did any of them who were new to the sport show talent enough that they could have played? Did any of them fall in love with the game and decide to play?
CA: The truth, which we were tuned into right away by our sports co-producer Sports Studio, is that it's easier to get real lacrosse players to do some limited acting rather than having actors play a lot of real-looking lacrosse. All the young men who play in the movie were lacrosse players first and some actually were or became promising actors. There was one Crooked Arrow who was a Hollywood actor who happened to be Native and we put him in goal (which still took considerable coaching). All the players were current or former college players with just a few exceptions. Stars Brandon Routh and Chelsea Ricketts had to be taught the little bit of lacrosse they played and had stunt doubles for the very little serious lacrosse they have to execute, though both learned the fundamentals and grew to enjoy the game.
Josh Rottman: Let's face it, most of the country is unfamiliar with lacrosse. What were the challenges in creating a major motion picture that would invite people who knew nothing about this sport to come enjoy Crooked Arrows?
CA: The movie has to be more than about lacrosse. Like any good sports movie, the actual story has to carry the day. We have a compelling and contemporary personal journey at the heart of our story for our lead that Brandon plays. We also think the movie takes people to a place most have never been — a Native American reservation. And that's what the best movies do: transport audiences.
David Herman in Cheektowaga, NY: How important is the sport's Native American ancestry to the film and how big was it for you guys to gain approval for the movie from those communities?
CA: Huge and huger. The Native American component of the film turned out to be the movie's secret sauce. We were so lucky to have Neal Powless and Ernie Stevens III there to make sure we got it right. Also, all the Six Nations players brought authenticity — in their play, their demeanor, their customs, and their singing! The Native aspect elevates the movie to a new level. Here's an important tip: don't be late to the movie — the opening is awesome.
Tom in Manchester: Will the film be screened in the UK, Australia, Japan and Europe? Will it be available on DVD?
CA: The film will be released around the world and should get substantial play wherever lacrosse is played. In certain other areas, we may not focus as much on the lacrosse in the marketing and let them discover the sport when they see the movie. The movie will be on DVD by the fall.
Jade Alyse in Cary, N.C.: Brandon, are you part Native American in real life?
CA: Brandon is part (a small part) Native American. Originally from Iowa, Brandon has some Kickapoo blood in him.
Jason Maxwell in Chicago: What was the biggest challenge to shooting and editing the lacrosse scenes?
CA: Shooting sports adds an entirely new layer onto movie making. Recruiting the right players, training them, choreographing the plays, and repeating them over and over for different camera angles — it all takes a tremendous amount of time. We brought in some deeply experienced camera guys, including our director of photography Daniel Stoloff (who shot Miracle) and several great sports cinematographers, including some NFL Films guys. Editors Danny Saphire and Bart Rachmil did a great job making the lacrosse look as cinematic as possible, which was a challenge further exacerbated when some of the wider-shot scenes of lacrosse had a lab problem and became mostly unusable. The key is allow newcomers into the game.
Jennifer Martin in Vero Beach, FL: Why did you choose lacrosse as the sport for this film and were any others considered?
CA: The script was actually written over 15 years ago but Hollywood didn't seem ready for a lacrosse movie. Producing partner Mitchell Peck who developed it with writer Todd Baird never gave up. It was always going to be a lacrosse movie. Every other sport has had its movie!
Jordan Johnson in Arlingon, Va: What was your strategy with the lacrosse game action in the film? Oftentimes Hollywood creates unnatural plays because they think it'll look better on screen. What line did you dance between accuracy and the technical side of lacrosse compared to something that'll look good on the big screen?
CA: Lacrosse is a tricky sport to film. The field is big. The players are behind helmets. The ball is small and white. (Ever notice why basketball is so easy to follow? The ball is huge an orange and you can see every player's face on the court which his relatively small.). The plays took a lot of choreography, which was accomplished by Jamison Koesterer (Johns Hopkins) and Neal Powless (Nazareth) working with Sports Studio's Mark Ellis. The original script had 77 lacrosse plays in it! That had to be cut down for practicality's sake. Every move was mapped, rehearsed and shot from at least one (and generally two/three angles). We did nothing but shoot lacrosse for nearly two weeks at the beginning of the shoot to get the players (who weren't actors) used to being on camera.
James Trent in Bangor, Maine: What's the general vibe toward lacrosse you guys are getting from sponsors, Hollywood people, etc.?
CA: Cautious from Hollywood. Certain sponsors totally get it. Reebok, of course. US Lacrosse, naturally. But then there are surprises; Moe's Southwestern Grill (434 stores) has decided to make an active approach to the lacrosse market. We had a lot of support from various products (Audi, Quiznos, Pizza Hut, Coke) but that was all product, which was nice but didn't pay the bills. Lacrossse products like Cascade were fantastic — 100+ helmets.
Mike Wiseman in Hoboken, NJ: What is the key to this movie having success?
CA: We need the lacrosse base to treat this movie the way the Christian community treated The Passion Of the Christ or the way the football/faith-based community treated Blindside. It has to be a movement. If the base comes (EARLY — FIRST WEEKEND) the word of mouth will spread and the general public will get it and come, and the gospel will spread.
Debbie Price in Timonium, MD: Brandon, not having had much experience with lacrosse before the movie what is your take on the sport now?
CA: Brandon was a soccer player in his early days growing up in Iowa and still plays. So it was good to have him established as an athlete. Watching Brandon wade into the sport — starting at last year's Final Four in Baltimore — was an experience. He was overwhelmed at the passion of the players and fans. He had endless hours of generous advice from lacrosse players on looking authentic with the stick.
Craig Miller in Lower Merion, PA: Funniest story/outtake from filming with all those crazy lacrosse players?
CA: Our Native players were the funniest. They are like the Harlem Globetrotters – always joking, always horsing around and all with great lacrosse. The funniest moment was probably when Coventry (opposing team) player Dylan Burke did a rap song spontaneously on the set with all the players around. It's on our website and will be in the closing credits!
Justin Waterman in Webster, NY: What would surprise people about how you shoot a movie?
CA: How freaking slow it is and how many people seem to be standing around ALL THE TIME!
And how there's constantly food around to get fat eating. Also, people would be a little surprised at how much planning goes into making a movie. Tons.
Johnny Miller in Upper Arlingon, OH: Did you watch any NCAA or MLL teams for style of play for either of your teams? Did you model how you played lacrosse in the film after any particular team?
CA: We watched a ton of lacrosse and had lax players from top colleges and pro programs participate. No one team modeled, necessarily, but having Neal from Onondaga and Jamison from Hopkins set the bar pretty high. Remember, these are supposed to be high school players.
Lisa Alvarez in Cherry Creek, CO: Do you think there should be a shot clock in college lacrosse?
CA: Yes. Stalling is boring.
Johnny Adams in Portland, Ore.: How important is the sport's Native American ancestry to the film and how big was it for you guys to gain approval for the movie from those communities?
CA: Huge and huger. The Native American component of the film turned out to be the movie's secret sauce. We were so lucky to have Neal Powless and Ernie Stevens III there to make sure we got it right. Also, all the Six Nations players brought authenticity — in their play, their demeanor, their customs, and their singing! The Native aspect elevates the movie to a new level. Here's an important tip: don't be late to the movie – the opening is awesome.
Joey R in Hamburg, NY: To Mike Banks: I'm really looking forward to seeing your performance on the big screen. With your great smile, charm and zany personality you are truly cast from the mold of a cinematic star. Are you pursuing a career in acting and if so what can we expect next?!
CA: Mike is doing some acting. He just finished a play. He was a great spirit on the set. We knew the minute we saw him at auditions he had to be in the movie.
Check out the movie in select theatres starting May 18, and nationwide and in Canada June 1. Go to CrookedArrows.com for theatre locations.


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E46 328i Header Install
First thing's first- Thank you Hamann330ci for having put together that writeup! And thanks Alex "Supermeng" for helping me out with this project!
Well I started late and I got caught by the night. I called it a night after having torqued down the front header. Tomorrow I will pick it up at torquing down the rear header and reassemble the car.
I got these headers on Ebay and were $113shipped. They are not perfect (the secondary o2 bungs pointing the wrong way so as for me not to be able to put oxygen sensors... I sense a CEL coming on upon startup lol), but other than that, they were in great shape and all. For the imperfections that they may have, really you cant complain given the price. The welds were solid and flanges thick, collector was smooth and on the inside any highspots on the welding were grinded down already (Makes one wonder if $1400 Supersprint headers are REALLY worth the difference?... but that's a subject for another thread).
On to the good stuff!
I must say the factory M52TUB28 headers are freagging disgustingly restrictive!!!! Their design is something I'd expect to see on a Cummins turbo deisel in the sense that it's a common log very short and leading into a single chokepoint for the tube, it's ridiculous! (not to mention WOW they were heavy!)
Cleaned off the headers with brake parts cleaner, then started painting them with DEI Silicone paint...
Once 2 layers of DEI silicone paint went on the headers, I wrapped them with DEI exhaust wrap as much as I could reach (Dont mind my toes, I was wearing "Jesus-Sandals" lol)
No headers in the engine bay (It's a BMW! you KNOW I had my Heinekens for the beer-breaks :thumbsup:)
Car as it sits right now
Tomorrow morning it should be finished up and I will post up pics soon as I can (I'm back at work tomorrow). I cant wait!!!
The install will be better than the removal. Goodluck
Thanks! Hey guys question!
What the heck do I do with the air pump? The writeup says nothing about re-installing it, but it also doesnt say for sure that I could throw it away. Also if I could leave it out, what do I do with the part that the hose goes to on the engine (the part that looks like it has a vacuum line going into it, at the front of the engine, to which goes the other end of the air pump's big hose)? Can that be just left open? I ask because I have no idea what the thing is. If I did I could figure it out and do as I please lol
Thanks for the help in advance!!!
not sure...when I did mine it was just hooking up the o2 sensors on them and taht was a bout it. Well minus the stuff removed for the install.
Anyways! Guys lesson learned lol. Some people get lucky with e-bay headers, and some do not. I was in the clear aside from the o2 bung issue from yesterday... until it came time to put on the engine mount... The DAMN PRIMARY sits too close! The writeup says that u may have to trim off some of the shield on the mount in order to get clearance but even with that it was waaay far off. Well I wasnt going to let that stop me. After all, Im the king of rigs around here in all my cars! Sooo I went downtown on the mount bracket with my grinder...
I actually went further than what this pic shows. I went to the top edge of that rivet just above where you see I grinded. And even STILL it was not fitting right (the bracket would not fit flush against the block at the top 2 bolts). It was lined up. So I thought ok... Im not going to force it because that's just asking to crack it.... AH!!! make some sort of spacer to go bet'n the bracket and the blockso that I could actually torque down the bolts with no fear of cracking the bracket!
One is in fact 3 washers superglued together just for ease to handle them when Im putting it into place (doing it with 3 individual washers would take me all day!), the other is actually a spacer for the Exhaust Gas Recirculator (EGR) of my old 95 Nissan Maxima (it pays off to keep all those misc parts!)
from the front
from the rear
Im not the type to whine and complain when something doesnt work. When Im this far into a project and I run into something, I MAKE it work at all costs :thumbsup:
Hey here's one good thing about these e-bay headers! The flanges on the rear lined up pretty easily! The one closer to the pass side needed some encouragement from my "master key" (a 2ft crow bar :thumbsup:) but it wasnt anything to require going to a muffler shop like some have had to do.
nice writeup
lol indeed. Driving impressions so far have been gathered with street driving. Tomorrow I will have PLENTY of highway driving on it so I will come back with a full impression tomorrow night. But so far, I have a rasp at 3000-3500 that it sounds like the Hondas are on the march, then from 3500-redline it sounds like automotive sex. Mind you that I still have the stock muffler. But so far, I like it!
Now all you need is a good exhaust and a good tune. The tune will get rid of your chk eng light and well it will optimize your headers so you don't run so lean. There will be a slight noise change after the tune but to me it was for the better. If you look enough on here you will get many great exhaust ideas. I personally have a Rouge Ikon and love it. Well enjoy those headers in the mean time!!!
After fixing that exhaust leak I had at the bottom flange... :thumbsup:. The Honda-attack that was going on at 3000-3500rpm is gone! It BEGINS to rasp around there but it's a nice rasp (like a milled down, M3 with no cats sort of rasp) so I like it. According to the buttdyno there is more power everywhere. Off the line the response is great, revs much more freely throughout the powerband, after 3500 it moves noticeably better than with stock headers/cats. But you also notice it on normal street driving. Overall, Im very impressed by them.
As of right now, this is how the underside of my car looks...
Middle (yes both resonators were removed prior to doing my baseline dyno)
I may go dyno it either tomorrow or next week Weds. Depends on how good it goes at work today. I will buy a new thumbdrive so I could get both the runfiles from my baseline and also the post-headers dyno to overlay them and see exactly, with SAE #s, what the headers alone did to the powerband.... ACTUALLY, I might as well wait for next week! I ordered an intake off of ebay (yes I know it's not for power, but just for laughs and giggles, it was only $45 shipped anyways, plus it's going to sound great along with the headers). So ok, next weds, I do 3pulls on headers alone, change my intake over to the ebay intake, and see what that does if anything (again, just for laughs and giggles).
Stay tuned!
Awesome write-up, pictures and feedback. Very encouraging for other looking to add headers to their car. :thumbsup:
You should do a true cold air intake, and not a short ram type. Make sure you have a good filter too, or it will foul your maf.
this one
But even still, like I said, it's not for power, it's for sound, so I dont care lol. It's all going to get changed around in a year so why complicate myself and spend more than what I have to ;). If you're curious as to what Im going to do with it... I miss this sound!!!! LOL This is a quick vid leaving a toll plaza when I had my Maxima on 6psi. At 9psi the turbine sound was just insane, I miss it :-P lol. But that's a conversation for another thread, on another day :thumbsup:
Great write-up!! Thanks for the helpful hits and pics. I just picked up a full ZHP cat-back and am getting 330 Headers from F1 Autohaus...can't wait!!
Great write up, excellent pictures and hats off to you, I would never attempt a DIY like that.:bow: One question. I have just ordered my headers, from ebay (paid a bit more:bawling:) and want to know. Does everyone wrap their headers? If so or not, why?
Not everyone wraps their headers. It is beneficial to do so, but it has it's drawbacks.
- Maintains the heat inside the tubing (greatly reducing under-hood temperatures)
- Promote scavenging effect by keeping the air hot and thus faster moving (due to rate of expansion of this hot air contrasted by a cooler temperature exhaust gas). On turbo'd engines wrap makes a big difference in spoolup times for example. On my Maxima I saw 700-800rpm QUICKER spoolup by just wrapping the exhaust leading up to the turbine
- It's made of fiberglass. If you have ever been up in an attic (insulation) or worked around boats, you may know that fiberglass (depending on how sensitive your skin may be) will cause you to itch like hell (doesnt do anything to me but a slight discomfort, but the forearms of the friend that was helping me looked like he allowed jellyfish to sting him LOL)
- DEPENDING on how you install the wrap, and the kind of metal the tube is made of, it may cause the pipe to corrode. Some people just buy headers, wrap them, and install them... WRONG! CLEAN the surface with brake parts cleaner and a shop towel; spray DEI silicone paint on the tubing to be covered by the wrap (this will act as a barrier in case moisture gets passed the wrap so it doesnt linger there on bare metal to rust it out); NOW wrap the tubing; after wrapping, go downtown with the DEI paint on the wrap itself (SOAK the paint into the fabric, this will act as an outer barrier to repel moisture for the most part from soaking the wrap and entering down to the metal). There you go.
This is in lameman's terminology here. If someone wants to nit-pick it and go at it with technical terminology go right ahead :)
Dyno update!!!
Well not bad!
That is my best baseline dyno run(#3 blue), Vs my best post-headers run (#5 red), both on SAE #s of course.
WHP- 174 to 180= 6whp
WTQ- 185 to 189= 4wtq
Notice that after 6000rpm, the baseline run's WHP line plateau'd. Now with the headers, it is actually still increasing power at redline.
WHP- 168 to 179= 11whp
WTQ- 136 to 145= 9wtq
From a Cost/Benefit Point of View-
Cost- Headers were $113shipped... that's it!
(redline) 11whp= $10.27/whp
Not bad! Especially with how ripped off the BMW client base is with some products just for the fact we drive BMWs, that so many companies think they can charge ridiculous prices.
It should be noted that the a/f mix is now much richer than before, so there is still WHP and WTQ to be gained from simple a/f tuning alone. Headers on this car (as with most other cars) are a great bolt-on, however to get the most out of it, they usually require some tuning.
From my experience tuning engines of various displacements, I could estimate that with air/fuel tuning alone this car could gain another 3-4whp at peak.
Hope this information helps someone out there! :thumbsup:
Something isn't right. You're car is not making optimal power at all, considering the stock manifold has a drop off past 6000rpm. I'd say a bit of tuning could get you more than 4whp...
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Routine traffic stop nets stolen TVs, other items
When Officer Peter Lennon approached the vehicle, he noticed three large flat-screen televisions, clothing and other items in the back of the silver Jeep SUV. Many of the items, said Chabot, still had anti-theft wrapping and security devices attached.Russo and her passenger, 29-year-old Hezekiah Mendoza, also of Manchester, couldn't account for where they obtained the three televisions, three chandeliers, Sony sound system and several clothing items, said Chabot."It was one of your typical low-risk motor vehicle stops, and lo and behold, Officer Lennon stumbled upon something much more significant," said Chabot. "The items were in plain view, and (Lennon) discovered more criminal activity than he anticipated."Due to lack of initial evidence proving the items were stolen, the suspects weren't arrested at the time, but the contents of the vehicle were seized.An investigation into the matter revealed the televisions, clothing and sound system were taken from Wal-Mart and the chandeliers were taken from Home Depot. Chabot said video surveillance captured the crimes, though he couldn't provide additional details.The stolen items were calculated to be worth more than $1,500 combined, and warrants were issued Wednesday for both Russo and Mendoza on charges of receiving stolen property, Class A felony offenses due to the value of the items.The same day they were pulled over in Auburn, Russo and Mendoza were each arrested around 1 a.m. and charged with possession of a controlled drug, according to Epping Police Chief Michael Wallace.