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I trust Ken Donat and Ken only. Just my 2 cents.
Hey everyone!
I know that this is a crazy week for most with Transworld and what not (hopefully the budget allows next year for us...but this year we're working hard to secure a permanent spot and our money is tied up with that...) but I have a quick question...
Anyone recommend a good place for commercial property insurance? You know, the year round-protect your assest and location type...
Or should I just look local?
I know we've gotten our event insurance recommended by others on here so I figured I'd give it a shot!
I trust Ken Donat and Ken only. Just my 2 cents.
We used him this year and he was great to work with! The mall we were at had very stringent rules and needs and he got it done for us with ease! That was for our event insurance for the month (setup and teardown too).
Does he do building and asset insurance too?
I thought he only did event insurance?
Just looked at the website...I see it now! I'll contact him soon!
Haha yup! He's the man, he does event insurance obviously but he owns westland insurance now
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Cardiology Research and Practice
Volume 2012 (2012), Article ID 789071, 7 pages
Endothelin-1 and Norepinephrine Overflow from Cardiac Sympathetic Nerve Endings in Myocardial Ischemia
1Laboratory of Pathological and Molecular Pharmacology, Osaka University of Pharmaceutical Sciences, Takatsuki, Osaka 569-1094, Japan
2Department of Pharmacology, Shiga University of Medical Science, Otsu, Shiga 520-2192, Japan
3Department of Pharmacy, Osaka Rosai Hospital, Sakai, Osaka 591-8025, Japan
Received 9 April 2012; Revised 14 May 2012; Accepted 15 May 2012
Academic Editor: Theofilos M. Kolettis
Copyright © 2012 Masashi Tawa et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
In protracted myocardial ischemia, sympathetic activation with carrier-mediated excessive norepinephrine (NE) release from its nerve endings due to reversal of NE transporter in an outward direction is a prominent cause of arrhythmias and cardiac dysfunction. Endothelin-1 (ET-1) and its receptors are intimately involved in the regulation of this carrier-mediated NE overflow in protracted myocardial ischemia. The ET-1 system is often complex, sometimes involving opposing actions depending on which receptor subtype is activated, which cells are affected, and whether stimuli are endogenously generated or exogenously applied. Therefore, a detailed understanding of the ET-1 system is important for applying drugs acting on this system in clinical settings for the treatment of ischemic cardiac disease. This article provides a detailed analysis of how the ET-1 system is involved in the regulation of carrier-mediated NE release from sympathetic nerve endings in protracted myocardial ischemia.
1. Introduction
Enhancement of cardiac sympathetic nerve activity in myocardial ischemia elicits norepinephrine (NE) release from its nerve endings. Activation of -adrenoceptors by NE causes positive inotropic and chronotropic effects which augment oxygen demand. By activating -adrenoceptors, NE also provokes coronary vasoconstriction, which diminishes oxygen supply. The detailed mechanisms by which NE regulates cardiac contractility or coronary vasomotion have been well described in previous reports [1–6]. Both of these actions of NE are considered to be important factors that exacerbate myocardial ischemia. Indeed, animal and clinical studies have demonstrated that negative modulation of NE release, or blockade of its effects, significantly suppresses postischemic cardiac dysfunction and arrhythmias [7–11]. The mechanisms by which ischemia enhances cardiac sympathetic nerve activity and increases NE overflow have been discussed [7]. In cardiac sympathetic nerve endings in a protracted ischemic condition, free axoplasmic NE and H+ accumulate massively owing to the lack of a driving force for NE storage by ATP depletion. Increased axoplasmic H+ activates the Na+/H+ exchanger (NHE), which consequently leads to an influx of Na+ in exchange for H+. Furthermore, inhibition of Na+/K+ ATPase activity due to ATP depletion results in the accumulation of axoplasmic Na+. This Na+ accumulation triggers excessive axoplasmic NE release via reversal of the NE transporter (NET) from the intracellular to extracellular space [6, 12]. This carrier-mediated NE release in protracted myocardial ischemia depends on Na+ entry via NHE activation and is supported by evidence that NHE inhibitors are as effective as NET inhibitors in reducing NE overflow [9]. Although several physiologically active substances (e.g., histamine, adenosine, bradykinin, and angiotensin) contribute to the modulation of this release via respective receptors [9–11], endothelin-1 (ET-1) is also one of them. ET-1 was originally found as a 21-amino acid vasoconstrictor peptide produced by vascular endothelial cells [13]. Accumulating evidence indicates the crucial role of ET-1 in the pathogenesis and/or development of several cardiovascular diseases [14]. It has been reported that an ischemic event results in increases in ET-1 levels [15–18] and its binding sites [19, 20]. Additionally, blockade of its effects has been shown to act protectively against postischemic cardiac and/or coronary dysfunction both in animal studies [18, 21–29] and human clinical trials [30, 31]. These findings suggest that ET-1 plays an important role in the pathophysiology of myocardial ischemia. In the following paragraphs, we will summarize the interaction between the ET-1 system and NE overflow from cardiac sympathetic nerve endings in protracted myocardial ischemia.
2. ET-1 System in NE Overflow
ET-1 is generated from an intermediate form termed big ET-1 via proteolytic cleavage by endothelin-converting enzyme (ECE) [13]. The prime sites of ET-1 production in the heart are coronary and endocardial endothelial cells [32–34]. This peptide is well known to have several cardiovascular actions through the activation of its receptors, endothelin type A receptors (ETARs) and type B receptors (ETBRs) [35]. Briefly, both receptor subtypes belong to the seven-transmembrane domain rhodopsin receptor superfamily, and signaling transduction of these receptors is coupled to multiple G-proteins (Gq, Gi/o, and Gs) [35]. These ET-1 receptors are widely distributed in the mammalian heart, such as the coronary vasculature [36], myocardium [37], and cardiac sympathetic nerve terminal [24].
2.1. ETARs in NE Overflow
Our previous study using the Langendorff technique indicated for the first time that ETARs modulate carrier-mediated NE release from cardiac sympathetic nerve endings [23]. In this report, we demonstrated that a selective ETAR antagonist ABT-627 markedly decreased NE overflow in coronary effluent after 40-min global ischemia and reperfusion in rat hearts. A similar result was reported by Isaka and associates [24], who found that ETARs blockade with BQ-123, a selective ETAR antagonist, significantly attenuated NE overflow during reperfusion after 20-min global ischemia in isolated perfused guinea pig hearts. In addition, they provided a definitive demonstration that ETARs exist in cardiac sympathetic nerve terminals of guinea pig hearts. These findings suggest that activation of ETARs existing in cardiac sympathetic nerve endings modulates carrier-mediated NE release in a stimulatory manner. As support for this proposal, we have reported that 40-min global ischemia-induced NE overflow was more highly observed in isolated perfused hearts of ETBR-deficient homozygous (sl/sl) rats than in hearts of wild-type rats, and an exaggerated response to prolonged ischemia in sl/sl rats was abolished by ABT-627 treatment, indicating that ETAR-mediated action is responsible for augmented NE overflow in sl/sl rats [23].
The signaling mechanism of ETAR in stimulatory modulation of carrier-mediated NE release has been suggested. As mentioned above, NHE is an important regulator for carrier-mediated NE release from sympathetic nerve endings in protracted myocardial ischemia [9]. This transporter activity is well known to be regulated by a variety of G-protein coupled receptor (GPCR) systems [38]. In fact, several researchers have clarified the positive functional coupling of ET-1/ETAR and NHE at a cellular level [39, 40]. Consistent with this view, in isolated perfused hearts, pharmacological NHE inhibition by 5-(N-ethyl-N-isopropyl)-amiloride (EIPA) has been demonstrated to decrease excessive NE release induced by ETARs activation [23, 24]. Therefore, it is reasonable to consider that ETARs stimulation activates the NHE system at the level of cardiac sympathetic nerves. On the other hand, the second messengers mediating this response remain unclear. Because phospholipase C (PLC)-protein kinase C (PKC) cascade is known to activate the NHE system [38], the stimulatory action of ETAR on carrier-mediated NE release may result from an increase in PLC and/or PKC activity. However, Horinouchi and colleagues recently demonstrated that there are multiple intracellular signal transduction pathways for ETAR to activate NHE [40]. Briefly, they provided evidence for the existence of an NHE activating pathway mediated through p38 mitogen-activated protein kinase (p38 MAPK), not through PLC, in Chinese hamster ovary cells. Unfortunately, at present, we cannot assert which pathway plays a critical role in the positive regulation of NHE activity via ETAR in cardiac sympathetic nerves. It is hoped that the detailed mechanisms of how ETAR stimulates the NHE system and, thus, carrier-mediated NE release in protracted myocardial ischemia will be clarified.
In the above-mentioned previous studies using isolated perfused hearts, NE overflow reflected the severity of cardiac dysfunction after reperfusion. For example, ABT-627 improved left ventricular systolic and diastolic function after myocardial ischemia/reperfusion in rat hearts [23]. Additionally, BQ-123 completely diminished the incidence of ventricular fibrillation after global ischemia in guinea pig hearts [24]. Furthermore, more severe left ventricular dysfunction after myocardial ischemia/reperfusion was observed in sl/sl rats than that in wild-type rats, and this severity in sl/sl rats decreased by treatment with ABT-627 [23]. Basically, ETAR-mediated NE overflow is considered to contribute, at least in part, to ischemia/reperfusion-induced cardiac dysfunction.
2.2. ETBRs in NE Overflow
It is still unclear whether or not ETBR directly interacts with carrier-mediated NE release. Our group and another group have confirmed that pharmacological blockade of ETBRs by A-192621 (selective ETBR antagonist) and BQ-788 (selective ETBR antagonist), respectively, exaggerates NE overflow induced by protracted global myocardial ischemia in isolated rodent hearts [23, 24]. As mentioned in Section 2.1, we noted that 40-min global ischemia-induced NE overflow in isolated perfused hearts of ETBR-deficient sl/sl rats was more highly observed than in hearts of wild-type rats. These responses to pharmacological blockade and the effects of genetic ETBRs deficiency were almost completely abolished by ABT-627 treatment, indicating the possibility that ETBR itself does not play an important role in carrier-mediated NE release in ischemic hearts [23]. On the other hand, another group has noted that treatment with the selective ETBR agonist sarafotoxin S6c suppresses NE overflow during reperfusion after 20-min global ischemia in isolated perfused guinea pig hearts [24]. More recently, we have demonstrated that ETBRs stimulation resulting from treatment with big ET-1 (see Section 2.5 for more details) suppresses NE overflow induced by 40-min global ischemia in isolated perfused rat hearts [41]. In contrast to the above idea, these findings indicate the possibility that ETBR negatively modulates carrier-mediated NE release from cardiac sympathetic nerve endings. The reason for this discrepancy may be due to differences between endogenous and exogenous stimuli. Briefly, the ability of ETBRs stimulation by endogenously generated ET-1 may be extremely low. As such, the role of ETBR on carrier-mediated NE release from cardiac sympathetic nerve endings during protracted ischemia is not completely clear and further study is required.
Although it is unclear whether or not there is a direct contribution of ETBR to carrier-mediated NE release during myocardial ischemia, the amount of NE released from ischemic hearts has reflected cardiac dysfunction in studies introduced in this section. Briefly, treatment with A-192621 worsened left ventricular (both systolic and diastolic) function during reperfusion after 40-min global ischemia, and this detrimental effect of A-192621 was completely abolished by concomitant treatment with ABT-627 in rat hearts [23]. In addition, S6c prevented reperfusion arrhythmias (both incidence and duration of ventricular fibrillation) in guinea pig hearts [24]. On the other hand, BQ-788 did not alter the duration of ventricular fibrillation after 20-min global ischemia in guinea pig hearts [24].
2.3. Endogenously Generated ET-1 in NE Overflow
As described above, we have demonstrated that treatment with ABT-627 with or without the combination of A-192621 markedly suppressed NE overflow induced by protracted global myocardial ischemia to the same level in isolated perfused rat hearts using the Langendorff technique [23]. Isaka et al. also showed that the nonselective ETAR/ETBR antagonist PD-142893 significantly attenuated carrier-mediated NE release during 20-min global ischemia in isolated perfused guinea pig hearts [24]. These findings suggest that endogenous ET-1 contributes to carrier-mediated NE release by exclusively stimulating ETARs in ischemic hearts. This proposal was supported by our recent study which investigated the effects of ECE inhibition [18]. In this study using Langendorff perfused rat hearts, we observed that the selective ECE inhibitor SM-19712 suppressed excessive NE release from sympathetic nerve endings during 40-min global ischemia.
In the previous study, we showed that cardiac ET-1 levels were reduced during ischemia in rat hearts [18]. However, this does not mean that ET-1-induced action is diminished during myocardial ischemia. This is because ET-1 levels in coronary effluent from postischemic hearts were slightly, but not significantly, increased in our subsequent research (unpublished data). In fact, the magnitude of increase in ET-1 release observed during myocardial ischemia has been well documented [15, 16]. Although it is unclear whether or not ET-1 synthesis is increased in ischemic hearts from our research results, there is almost no doubt that the release of this peptide is increased. Released ET-1 during protracted myocardial ischemia may play an important role in carrier-mediated NE release via the activation of ETARs. Unfortunately, we did not check the effect of SM-19712 on ET-1 levels in coronary effluent from postischemic hearts. However, we have confirmed that cardiac ET-1 levels are not different before and immediately after prolonged ischemia in the case of SM-19712 treatment [18], suggesting the possibility that ET-1 release during myocardial ischemia is reduced by ECE inhibition. Taken together, endogenous ET-1 positively regulates protracted ischemia-induced NE overflow via the activation of ETARs, although it is unclear whether or not ET-1 is newly synthesized during ischemia.
Regarding cardiac function, PD-142893 and SM-19712 respectively shortened the duration of ventricular fibrillation [24] and improved left ventricular function [18] during reperfusion after myocardial ischemia relative to NE overflow. Therefore, endogenously generated ET-1 seems to be able to promote postischemic NE overflow, and this contributes, at least in part, to subsequent cardiac dysfunction.
2.4. Exogenously Applied ET-1 in NE Overflow
Exogenously applied ET-1 induces the same effects as endogenous ET-1 on carrier-mediated NE release from cardiac sympathetic nerve endings in ischemic hearts. In our study using isolated perfused rat hearts, exogenous ET-1 (0.03 and 0.1 nM) caused a marked and dose-dependent increase in NE overflow induced by 40-min global myocardial ischemia. Moreover, this action of exogenous ET-1 (0.1 nM) on NE overflow was completely suppressed by treatment with ABT-627 or EIPA [23]. In accordance with our findings, Isaka and associates also obtained results indicating that carrier-mediated NE release induced by 20-min global ischemia was augmented by exogenous ET-1 (0.1 and 1 nM) in a dose-dependent manner and this augmentation was counteracted with the combination of EIPA in isolated perfused guinea pig hearts [24]. Collectively, it is suggested that exogenously applied ET-1 positively regulates carrier-mediated NE release, possibly activating the NHE system through ETARs stimulation in protracted myocardial ischemia.
Exogenously applied ET-1 worsened cardiac dysfunction during reperfusion after global ischemia in association with the amount of NE released from ischemic hearts. In our study using isolated perfused rat hearts, exogenous ET-1 produced severe left ventricular systolic and diastolic dysfunction after ischemia/reperfusion in a dose-dependent manner, but this response was markedly suppressed in the presence of ABT-627 or EIPA [23]. Also, in the report by Isaka et al., exogenously applied ET-1 prolonged the duration of ventricular fibrillation in reperfusion in guinea pig hearts. Furthermore, ET-1-induced ventricular fibrillation was completely diminished by the combination of EIPA [24].
2.5. Exogenously Applied Big ET-1 in NE Overflow
It is well known that big ET-1 itself has no physiological effects independent of its conversion into ET-1 [42, 43]. Therefore, exogenously applied big ET-1 is thought to have qualitatively the same biological activities as ET-1. In our recent study using isolated perfused rat hearts, however, exogenous big ET-1 (0.1, 0.3 and 1 nM) did not increase NE overflow induced by 40-min global myocardial ischemia as opposed to the case of exogenously applied ET-1, in spite of the fact that ET-1 levels in coronary effluent from the heart exposed to protracted ischemia were dose-dependently increased by exogenous big ET-1 application [41]. To be more precise, a middle dose of this precursor peptide (0.3 nM) has a significant inhibitory action on NE overflow in ischemic hearts. This action was markedly attenuated by treatment with SM-19712 or A-192621, suggesting that exogenously applied big ET-1 is converted to ET-1 by ECE, locally in the heart, and this ET-1 binds to ETBRs to exert its related beneficial action. However, it is important to note that the dose-response curve of the exogenous big ET-1-induced depressive effect on NE overflow was bellshaped (0.3 > 1 > 0.1 nM). One of the possible reasons is that ETBRs may already be saturated by treatment with a middle dose of big ET-1, considering the result that combination of exogenous big ET-1 (0.3 nM) and ABT-627 did not produce a synergetic effect on NE overflow. Briefly, it has been proposed that a certain amount of ET-1 generated from exogenously applied big ET-1 preferentially acts on ETBRs, but excessively generated ET-1 acts also on ETARs in ischemic hearts. We hypothesize functional coupling of ETBRs and ECE-1, a dominant subtype of ECE, as for the reason why this phenomenon occurs. ECE-1 is classified into four isoforms based on differences in subcellular distribution [44]. Emoto et al. described that the isoform cleaving big ET-1 is different between endogenously generated and exogenously applied ET-1; the former is mainly catalyzed by isoforms expressed intracellularly, whereas the latter is cleaved by those expressed on the cell surface [45]. Based on this paper, endogenous ET-1 should be mostly generated inside the cell, whereas exogenously applied big ET-1 may be cleaved at the cell surface. In short, this isoform expressed on the cell surface would be positionally and/or functionally coupled to ETBRs. This is just a hypothesis and must be further investigated.
As mentioned above, although ETBRs have been demonstrated to exist in cardiac sympathetic nerves [24], it is unclear whether the effect seen at the middle dose (0.3 nM) of exogenous big ET-1 is through the activation of ETBRs existing at this site. However, this may not be the case because the exogenous big ET-1-induced inhibitory effect on NE overflow after 40-min global ischemia/reperfusion was completely cancelled by treatment with the nitric oxide (NO) synthase (NOS) inhibitor -nitro-L-arginine (NOARG) [46]. This finding suggests the involvement of NO derived from NOS in ETBR-mediated inhibitory modulation of carrier-mediated NE release. Although there are three different isoforms of NOS, neuronal NOS (NOS1), inducible NOS (NOS2), and endothelial NOS (NOS3), none have been confirmed to be normally distributed in sympathetic nerves [47, 48]. Therefore, ET-1 generated from exogenously applied big ET-1 is expected to bind to ETBRs existing in cells other than sympathetic nerves, for instance endothelium, cardiomyocyte, or nitrergic nerves. Further studies are required to clarify the role of ETBRs existing in cardiac sympathetic nerves in carrier-mediated NE release.
There are a number of possible mechanisms for negative modulation of carrier-mediated NE release by NO. As noted above, carrier-mediated NE release from cardiac sympathetic nerve endings is triggered by inhibition of ATPase activity due to ATP depletion and activation of NHE [12]. In this regard, NO has been demonstrated to improve Na+/K+ ATPase function [49] or inhibit NHE function [50, 51] under cardiac pathological conditions. On the other hand, in culture experiments using PC-12 cells, another investigation has shown that NO negatively modifies NET activity in sympathetic neurons by nitrosation of regulatory sites on the transporter [52]. Again, further research is required to identify how NO suppresses carrier-mediated NE release from cardiac sympathetic nerve endings in protracted myocardial ischemia.
The inhibitory effect of exogenous big ET-1 on NE overflow (0.3 > 1 > 0.1 nM) correlated well with the recovery of left ventricular systolic and diastolic function after ischemia/reperfusion in isolated perfused rat hearts [41]. Briefly, big ET-1 at a concentration of 0.3 nM most efficiently improved left ventricular dysfunction after reperfusion. In addition, this beneficial effect of exogenously applied big ET-1 was canceled by respective treatment with SM-19712, A-192621, and NOARG [41, 46].
3. Clinical Implications
It is impossible to directly apply the above findings to a clinical setting mainly because of ex vivo data. However, previous in vivo studies of myocardial ischemia in animal models have provided clinically relevant information [25–29, 53]. In accordance with ex vivo data, each of the selective ETAR antagonists [26, 28], the nonselective ETAR/ETBR antagonist [25, 27, 28] and the ECE inhibitor [29] have been reported to suppress increases in NE levels resulting from myocardial ischemia. For example, Fraccarollo et al. [26] demonstrated that long-term treatment with the selective ETAR antagonist LU135252 decreased plasma NE concentrations 12 weeks after proximal left coronary artery ligation in rats. Lee et al. [28] showed the inhibitory effect of the selective ETAR antagonist ABT-627 or nonselective ETAR/ETBR antagonist bosentan on regional myocardial interstitial and left ventricle NE levels 4 weeks after myocardial infarction induced by ligation of the anterior descending artery in rats. In this study, these ETR antagonists improved left ventricular systolic and diastolic function in postinfarcted rats. Also, in a study by Mulder and associates [25], bosentan decreased plasma NE levels in rats subjected to permanent left coronary artery ligation for 2 or 9 months. Likewise, Kolettis et al. [27] reported that bosentan markedly decreased serum NE levels 24 h postligation of the left coronary artery as well as the total duration of ventricular tachyarrhythmias during the delayed phase (1–24 h) postligation in rats. In addition, an orally active ECE inhibitor PP36 has been indicated to suppress cardiac tissue NE release 48 h after acute myocardial ischemia due to microsphere embolization of coronary microcirculation in rats [29]. Left ventricular contractility was partially restored and distention significantly improved by PP36 treatment in this research. Furthermore, an in vivo study using a genetic model was also consistent with the results of an ex vivo study. Oikonomidis et al. [53] recently demonstrated that serum NE levels during the early phase of myocardial infarction induced by left coronary artery ligation were much higher in ETBR-deficient sl/sl rats than in wild-type rats. In this study, the severity of ventricular tachyarrhythmias during the 1st h postmyocardial infarction was also greater in ETBR-deficient rats, indicating that ETBR decreases sympathetic activation and arrhythmogenesis during the early phase of myocardial infarction. Taken together, ETAR antagonists or ECE inhibitors can be expected to suppress sympathetic overactivity with excessive NE release and following cardiac dysfunction in patients with ischemic cardiac disease. As a matter of course, however, we must keep in mind that NE overflow is only one of the risk factors for the development of cardiac injury, and also that ET-1 possesses many other pathophysiological actions. In other words, although this paper focused on functional myocardial damage caused by ischemia, we should not forget that morphological alterations such as infarction, hypertrophy, apoptosis, or fibrosis are also contributive to myocardial ischemia/reperfusion injury.
4. Conclusion
In summary (see Figure 1), during protracted myocardial ischemia, endogenously generated or exogenously applied ET-1 activates ETARs in sympathetic nerve endings and stimulates neuronal NHE. As a result of NHE stimulation, NE is excessively released by potentiating carrier-mediated efflux. In contrast, ET-1 produced by appropriate amounts of exogenous big ET-1 works to prevent NE overflow by preferentially binding to ETBRs located on NOS containing cells and producing NO. On the other hand, the role of ETBR at cardiac sympathetic nerves in carrier-mediated NE release remains to be determined. Finally, a better understanding of the ET-1 system in NE overflow induced by protracted myocardial ischemia can lead to better treatments for ischemic cardiovascular diseases.
The authors thank Daniel Mrozek for reading the paper.
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Lima, OH Tonight, the young Barons just didnt have enough gas in the tank to hang in there with cross town NAIA rival UNOH as they dropped the home opener 110 to 53.
The Racers shot 50% from beyond the arc and out rebounded the Barons 48 to 30. Leading the way for the Racers offensively was Josh Vorst who netted 20 points for the game.
The Barons were led by freshman Aaron Kimbrough of Lima Central Catholic who netted 11 points while shooting 5 of 13 from the field and 1 for 1 from the charity stripe. Also contributing with double digits was sophomore, Chuck Patterson of Allen East who netted 10 points going 2 for 5 from the field and 6 for 10 from the line.
The Barons go on the road for their next two games before returning home on November 25th for an ORCC matchup with UC Clermont, tip off is set for 7:30pm. Come out and support your Barons, admission is free to all OSU Lima/Rhodes State students, faculty, and staff!


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"Where Has Grandpa Gone?"
Momfidence columnist Paula Spencer on coping with a parent with Alzheimer's
By Paula Spencer
Special Offer
"Hi, dad! It's Paula. How are you?"
"I'm fine, how are you?"
"We're fine. It's sunny and the girls are all outside. Henry's playing his guitar."
"Oh, that's good. And how's the weather?"
"Cool and sunny. How about down there?"
"The sun is shining. How's the family?"
"We're good. Next time we see you, we'll get Henry to play for you."
"Oh, nice, what instrument does he play?" "Guitar." "Oh, that's good…So how's the weather by you?" 'Round and 'round we go. There's an old saying in the Midwest, where I grew up: "If you don't like the weather, wait a few hours." On the phone with my dad, it's more like, "If you don't like the weather, wait a few seconds and pretend it's better." I could alternate saying it's raining, snowing or hailing all in the same conversation, and he'd respond to each new weather report as if he were hearing it afresh.
Because in a way, he is. Dad has dementia. We don't know whether it's Alzheimer's or vascular dementia (the kind often caused by small strokes) or what. My four kids' only other living grandparent, "Mima" (my mother-in-law), has dementia too, as did the only great-grandparent they ever knew. No wonder my son once said, "What's that thing Grandpa has? Old-timer's disease?"
Alzheimer's disease is not, of course, the inevitable fate of "old-timers." But millions of kids—and their parents—are feeling similarly flummoxed by their changing loved ones. Every family seems to have a story about a granddad who went to the store for bread and was found two states away. Or an aunt who hoards cat food, even though she no longer owns a cat. Mima once saw a 6-foot rabbit in her backyard. (And says she called the police over it, though the call was as imagined as the rabbit.)
"Where has Grandpa Gone?"
The very young tend to be oblivious to memory loss, wandering, delusions and the other behavioral changes of Alzheimer's. (Kind of like Grandpa himself.) "Can we catch it?" my youngest once asked—a reasonable question about an affliction with the word disease in its name. I said no, and borrowed an answer from geriatric consultant Joyce Simard, MSW, author of the children's book The Magic Tape Recorder: "It's like Grandpa had a tape recorder in his head, but it's turned off. When he was younger, the tape recorder was on, so he remembers more things from far back in his past." My oldest three, though, are old enough to feel they've lost a past relationship, while not knowing what to make of this new one.
For years, Grandpa called his beer "Power Ranger soda," a name Henry gave it at age 3 because of the design on the label—their private joke. Not anymore. No more year-round valentines from Mima, either. A beloved elder's blank stares or loud, circuitous questions can be deeply uncomfortable to a self-conscious teenager who can find mortification in something as benign as my nerdy shoes.
I don't believe in forcing kids to interact with their sick elders. If they volunteer a goodbye hug, I'm proud; if not, that's fine, too. And I don't usually hand over
the phone for merry-go-round conversations. My dad and mother-in-law don't even remember visits a few hours later. We grownups aren't let off so easily. November is National Alzheimer's Disease Awareness Month, but it may be time for a new name. Awareness isn't the problem; coping day-to-day is. How handy, at least, that dealing with aging parents is a bit like parenting in reverse. It starts around prickly adolescence, with the first clash over independence. ("I can drive!"…"I'm fine home alone!"…"Mind your own business!") Then come the taking-them-places years, if now to the doctor's instead of soccer and piano lessons, then the keeping-an-eye-on-them years.
Eventually, it's down to keeping them safe and avoiding tantrums. Last comes the phase requiring the skills you learned first: feeding, bathing, diapering, soothing. It's not a perfect parallel. But at least the terrain becomes more familiar. Certain child-rearing tactics transfer especially well:
Lamaze breathing
When my kids ask the same question over and over ("When will we get there?") I do some deep inhales-exhales to derail my slowly…building…exasperation—at least until the sixth or seventh time, when I feel free to holler, "Not soon enough!" With Dad, my panting manages to stave off hyperventilation until the 10th repetition—then I start talking about the weather and hope he forgets what he was asking.
Tempering expectations
Yes, not losing your temper is tough when your patience is fried, but just as I once pored over baby milestone charts (and thus learned I can't expect perfect table manners from a 1-year-old who doesn't yet have the motor skills to hold a fork), I boned up on the progressive stages of Alzheimer's. It's the disease that snatched up all the children's toothbrushes, one by one, and hoarded them in Grandpa's toiletry kit. It's the disease that chooses the same stained shirt day after day. Just like the developmental phase that kept my son in the same Davy Crockett getup for, oh, the entire time he was in preschool.
Taking it one day—er, one minute—at a time
Diaper-smell happens. Shoes get lost. Questions are asked. (Many, many, many, many questions.) Bedtime routines can last longer than a SpongeBob SquarePants marathon.
My brother and sister-in-law, a.k.a. the saints with whom my father lives, also look after her parents, and have six kids under 12. To cope, they rely on a brilliant motto that must be tattooed on their hearts: In with the moment. In the moment is where Dad hangs out. Arguing and correcting only add to the confusion and frustration someone with dementia feels. It's less frustrating for everyone to simply join him in the moment. So what if he mistakes the moon documentary on cable for a news report about a new lunar landing? So what if he insists the house where he grew up is still standing, though he just saw the photos of when it was bulldozed years ago? So what if he repeats a long, word-for-word anecdote two minutes later…and five minutes later…and seven minutes later?
Just be in the moment with him. Moments pass quickly enough, anyway. Kind of like the weather. Or raising kids.


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12 Jun 2014
FEES FROM WORK conducted for non-audit clients provided firms with the largest growth in income for 2012-2013, according to FRC figures.
PwC, KPMG, EY and Deloitte saw 5.8% growth in this area, while their overall growth slowed to almost half that of the previous year, at 3.9%. This compares to a total increase in fees of 7.7% in 2011-2012.
Further reading
The largest firms outside of the Big Four had their best performance in the last five years in 2012-13, with a 2.6% increase in total fees, Key Facts and Trends in the Accountancy Profession revealed.
Fees from non-audit clients climbed by 5.7% for mid-sized firms, offsetting a reduction in audit fee revenue of 1.7% and a 0.5% decline in non-audit work conducted for audit clients.
The Big Four continued to dominate across all areas, with a 2.8% increase in revenue from audit work.
However, the group saw a 3.2% fall in income from non-audit work for audit clients, following debate over conflicts of interests in audit contracts.
Elsewhere in the report, the FRC found membership of accountancy bodies continued to grow, rising 2.7% from 2009 to 2013 to 327,000 members in the UK. The number of students increased by 1.6% in 2013 to 167,000 UK-based trainees.
FRC executive director for conduct Paul George said: "It is clear from the report that the profession remains attractive with the number of students and new members indicating there is a good flow of bright, young accountants coming into the profession who will be able to support our economy in the years to come."
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If budgeting is to have any value at all, it needs a radical overhaul. In today's dynamic marketplace, budgeting can no longer serve as a company's only management system; it must integrate with and support dedicated strategy management systems, process improvement systems, and the like. In this paper, Professor Peter Horvath and Dr Ralf Sauter present what's wrong with the current approach to budgeting and how to fix it.
In this white paper CCH provide checklists to help accountants and finance professionals both in practice and in business examine these issues and make plans. Also includes a case study of a large commercial organisation working through the first year of mandatory iXBRL filing.


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Current Time
Concierge.com's insider take:
This comfy beachfront inn is a beloved home base for exploring historic English Harbour. Set on ten acres of wooded beachfront, the hotel has an infinity pool, as well as its own private crescent-shaped beach. The 34 roomsall with cathedral ceilings, mahogany four-poster beds, dark wood floors, terraces, and crisp white linensare housed in one- and two-story buildings. Four suites are right on the beach. The Stone Bar library/lounge and Terrace Restaurant serve afternoon tea and rum punch at sunset. Free water taxis shuttle guests to nearby Nelson's Dockyard.
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sand flea, also called sand hopper, beach flea, or beach hopper, any of several terrestrial crustaceans of the family Talitridae (order Amphipoda) that are notable for their hopping ability. The European sand flea (Talitrus saltator), which is about 1.5 centimetres (0.6 inch) long, lives on sand beaches near the high-tide mark, remaining buried in the sand during daytime and emerging at night to forage for food. Like other sand fleas, it feeds on organic debris.
The long-horned sand flea (T. longicornis), which is found on the Atlantic coast of North America from New England to the Gulf of Mexico, is named for its antennae, which are as long as the body. It grows to 2.5 centimetres (1 inch) long and is waxy white. In habit it resembles T. saltator.
The common sand flea (Orchestia agilis or O. platensis), which is found on the coast of Europe and on the eastern Atlantic coasts of the Americas from Greenland to Argentina, is about 1 centimetre (0.4 inch) in length and is mostly dark brown or gray; the tail is bluish, and the antennae are reddish brown. It lives in damp sand.


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She didnt call that woman a nigger.
She simply said that everywhere you look in the black community, all you
hear from them is NIGGER NIGGER NIGGER. or WHINE WHINE WHINE. Take
your pick.
So in essence, she was saying that they were the racists, not us.
Besides the fact that the caller admitted marrying inter racially, but
then complaining about the inevitable backwash. Which was a decision
she made, not anyone else.
Naturally, the basic facts of the case got lost in the mayhem.
Translated Moral of story: Only whites can be racists. And only white racism is bad.
This reminds me of the Rush Limbaugh/ Donovan McNabb story in which Limbaugh simply
said McNabb was a mediocre NFL player, but was given higher status because he
was black. Which has been proven more or less correct.
In essence, he was calling other people the racists, but naturally like anything
else remotely requiring intellectual comprehension, it was swallowed up in emotion.


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Tag Archives: Naps
If Only…
Leave a commentJune 4, 2012 by themommahen
You're not going to believe it, but sickness has once again darkened our door. Yes, with the arrival of summer …
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To Sleep, Perchance to Eat
Leave a commentMay 17, 2012 by themommahen
I've written about this before. How H#3 suffers some of the stereotypical treatment of beyond-second-borns. But I've now learned, and …
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Definitely the Third Child
Leave a commentDecember 4, 2011 by themommahen
See the full gallery on Posterous Perhaps we're not quite ready to go to one nap. Or perhaps we are …
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Add Chicken Stylist to My Resume
2May 18, 2011 by themommahen
This past weekend was awesome. Hatchling #1 found a four-leaf clover. In my entire life I have never found one. …
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Momma Knows Best
Leave a commentApril 20, 2011 by themommahen
This is how my 3yo flopped in protest of taking a nap. Asleep in less than a minute.


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Welcome to the Liberty, Missouri Farmers' Market 100% Vendor Grown!!
Wednesday mornings 7 till noon Located at 1332 West Kansas in Liberty, Mo (FELDMANS Farm & Home parking lot)
All our products are locally grown on farms around the northland.
There are many organically grown fruits and vegetables for you to choose from.
Also flowers and plants.
Just about anything in season can be found here!!
Come'on up to the Northland and enjoy the leisurely shopping experience in historic Liberty, Missouri.
(Photos by Gieselle Fest) Contact: email@example.com


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- Dec 10:
- Mall of America's 'Clouds' singalong benefit draws more than 5,000
- Nov 29:
- Zach Sobiech passed away in 2013, but in many ways he's still here
- Apr 30:
- Zach Sobiech's mom's book - silver linings after 'Clouds'
- Dec 21:
- Zach Sobiech's legacy is much more than 'Clouds'
- Dec 18:
- Zach Sobiech named one of CNN's 'extraordinary people' of 2013
- Dec 5:
- 5,000 sing Zach Sobiech's 'Clouds' in his memory at Mall of America
- Sep 19:
- From Zach Sobiech's 'Clouds,' U cancer fund gets $568,000
- Jul 23:
- Zach Sobiech's mom signs deal to write inspirational story titled 'Clouds'
- May 23:
- Zach Sobiech funeral: Mourners sing 'Clouds' to bid him farewell
- May 20:
- Zach Sobiech's farewell song 'Clouds' touched millions around the world
- May 9:
- Lakeland: Zach Sobiech's 'Clouds' inspires covers, celebrity tribute video
- Dec 8:
- Lakeland teenager with rare cancer saying goodbye through song (w/ video)
It's been almost a year since Zach Sobiech became an Internet sensation shortly before dying of a rare form of bone cancer.
But Sobiech, the Lakeland teenager who wrote "Clouds," continues to touch people with his story and his music.
Now, fans will have a chance to own a collection of music and videos from Sobiech and his band, A Firm Handshake.
"Fix Me Up: Deluxe Edition," a two-disc CD/DVD set, will be released May 6. Pre-orders are being taken on Amazon.com for $12.54.
In fall 2012, Sobiech was suffering from terminal osteosarcoma, when he wrote and performed "Clouds" as a farewell to family and friends. It has received more than 10 million hits on YouTube.
Days after his death on May 20, "Clouds" became the No. 1 rock song in the country, according to Billboard magazine. It also reached No. 1 on iTunes -- and stayed at the top of the charts for four days.
Proceeds from the sale of the song and YouTube views are donated to the Zach Sobiech Osteosarcoma Fund through the Children's Cancer Research Fund. Scott Herold, CEO and founder of Rock the Cause, which released Sobiech's album, said the fund should top $1 million by the time "Fix Me Up: Deluxe Edition" is released.
Sales of "Clouds" remain strong, particularly in Latin America and Europe, Herold said.
"There are 7 billion people on the planet, and many of those people are still figuring out ways to hear Zach's music and hear his story," he said.
"Fix Me Up: Deluxe Edition" includes a new acoustic version of "Clouds" and a track of the largest "Clouds" choir at the Mall of America, Herold said. It also features "How to Go to Confession," a new single by Sobiech's longtime friend and songwriting partner, Sammy Brown. The DVD includes five videos.
The set will sell for $12.99 in stores such as Best Buy, Walmart and Barnes & Noble starting May 6. The release date coincides with the publication of "Fly a Little Higher," Laura Sobiech's inspirational book about her son, which is being published by Thomas Nelson, a Christian bookseller.
May 3 would have been Zach Sobiech's 19th birthday.
Mary Divine can be reached at 651-228-5443. Follow her at twitter.com/MaryEDivine.
The "Fix Me Up: Deluxe Edition" CD/DVD by A Firm Handshake can be pre-ordered now at georiot.co/1p8n.


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Michigan DUI Attorney
Refusing to Submit to the Breath Test
Call Now: 734-507-1333 or call our Toll Free, 24-hour Hotline at: 877-MY-CRIME (877-692-7463) |
If you are arrested for drunk driving, you will be taken to the police station for booking. Once you are there, the police officer will ask you to submit to a breath, blood, or urine test to determine your blood alcohol level. In most cases, you are asked to take a breath test. If you refuse to submit to the test they ask you to take, then a REPORT OF REFUSAL form will be sent to the Secretary of State, telling them that you refused to take the test. You will have only fourteen days from the day of your alleged refusal to contest the allegation. If you fail to contest your alleged refusal, the Secretary of State will add 6 points to your driving record and suspend your driver license for a one-year period! This action can be taken against you even before you go to court to address your drunk driving charge. Since the State (and not the court, itself) would take this drastic action against you, what takes place in court could play little or no role in what happens to your license when you refuse the officers request to take a breath test. As a matter of fact, it is even possible to be found NOT GUILTY in court and still have your license suspended for one year by the State for allegedly refusing the breath test!
Because of the extreme consequences for refusing to take a chemical test, you must fight this every step of the way. YOU MUST SUBMIT AN APPEAL WITHIN FOURTEEN DAYS OF YOUR ALLEGED REFUSAL TO AVOID LOSING YOUR LICENSE FOR ONE YEAR AND HAVING SIX POINTS ADDED TO YOUR DRIVING RECORD. If the appeal is received by the Secretary of State in a timely fashion, no action will be taken against you. Instead, a hearing date will be sent you, where you and your lawyer can defend against the officers allegation that you refused to take the breath test he or she offered you. The name of this hearing is called an IMPLIED CONSENT HEARING. At the hearing, only four issues matter:
- Did the police officer have reasonable grounds to believe you committed the crime of drunk driving or another related offense? (See MCLA 257.625( c ) (1) for the other offenses that are included in this issue)
- Were you placed under arrest for drunk driving (or another drunk-driving related offense listed in MCLA 257.625( c) (1))?
- Did you reasonably refuse to submit to the chemical test offered to you by the officer?
- Were you advised of your chemical test rights?
At Your Implied Consent Hearing
If the OFFICER fails to prove any one or more of the four issues listed above, you will win the hearing and no action will be taken against your license. Keep in mind that the officer carries the burden of showing all four of these issues. It is not your job to prove these four issues have not been met. You are not required to disprove anything! You must only attempt to show that the officer has failed to meet one or more of the four issues he is required to show at the hearing. On the other hand, if the officer does prove, by a preponderance of the evidence, (namely, 51%) that all four of these issues has been satisfied, you will lose your license and have six points placed on your record. You must challenge every one of these issues, through your lawyers questioning, in order to avoid losing your license for one year.
Succeeding at the License Refusal Hearing
You and your lawyer should be familiar with the possible legal issues that can be used to defend you at the hearing. Some of the tips and tactics below should be considered when preparing to fight your alleged refusal. What follows is only a partial list of possible tips and tactics that can be used in your defense. To get a more thorough analysis of your case and possible defenses for your "refusal" hearing, make sure to contact an experienced attorney.
The Basics about Legal Wins
The Law Office of Joseph F. Awad is
Michigan's Premier Drunk Driving Defenders.
The Law Office of
Joseph F. Awad, P.C. specializes in Criminal Defense of Michigan Drunk Driving OWI OUIL DUI Charges. Aggressive and Experienced, Attorney Awad will fight for
your rights.
If you are facing a drunk driving charge or breath test refusal hearing, get a FREE consultation for your case. Just complete the form below and submit it. The firm offers statewide representation. You can also contact us by visiting our Farmington Hills Office:
Click Here for Maps & Directions
26677 W. Twelve Mile Rd. Suite 100
Southfield, MI 48034
We Can Help | Michigan Drunk Driving Laws | Michigan Criminal Law | Counties Defended in Michigan
Michigan DUI Laws | Michigan DUI Penalties | License Restoration MI
© 2004-2009 Attorney Joseph Awad, Esq. | 26677 W. Twelve Mile Rd. (Suite 100) Southfield, MI 48034 | Oakland County, Michigan
Disclaimer: The information you obtain at this site is not, nor is it intended to be, legal advice.Please consult an attorney for individual advice regarding your own situation.


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Goggles, the new Google search engine for mobile phones
December 11th, 2009 | Published on: News
Google just announced the launch of Goggles, which if continues to be developed, without a doubt it'll change the concept of internet search. For now, it's only available for the Android systems, and it can be bought over the phone accessing AndroidMarket.
This new application "recognizes" a photo taken with the mobile phone camera and starts an automatic search regarding the content, with no need to introduce any word. Using different tools to explore the image, the program will immediately give us the most relevant searches.
As regards places, Goggles doesn't even need the photo. With only focusing the camera on the place from which we want information, whether it is a monument or a store, and leaning on the GPS, this tool will provide us with all the information.
At the moment, Google Goggles has a limited use to places, books, contacts information, works of art, monuments, whines and brand logos, but in the future, it is estimated that it will identify food, animals, plants, and even suggest chess moves, taking into account the disposition of the pieces on the table.
This is a new effort by Google to keep on innovating. Regarding the images, it was already launched during the current year, Similar Images and then Image Swirl, which is a search engine that gathers the results based on the contrast similarities, color and the position of the objects.
The new technology, especially its potential more tan its current use, has caused more than one to be alert. Based on the assumption that Goggles will evolve till being able to identify people, many wonder what is the limit. Although the information collected by Goggles is protected by Google's privacy policy, it can't be assured how the giant internet uses it or will use it.
This way, Google adds to Google Maps, Froogle, Google Book Search, Google Earth, Google Scholar, Talk, Video and News, a new application that promises revolutionize the way to search on net of networks, even when it will cause a lot of controversy what will be the use of the information given.
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This is a discussion on Not using social media means your crazy? DailyNews article, ridiculous! within the Off Topic & Humor Discussion forums, part of the The Back Porch category; Originally Posted by kapnketel Its not just FB, its anything you put on the net. Try googling your forum name and see what comes up. ...
Ironic that the HR department may think you are crazy, yet according to a survey by CEO magazine last year only 4% of the CEOs of Fortune 500 companies have FB profiles. Why?, FB content is 99% useless blather. I am a high tech executive who started my own company a few years ago after taking early retirement as an executive of a Fortune 500 tech firm. I use Linked In extensively and blog because I get a great value out of it. I do not use Facebook because I do not care what you had for breakfast this morning and have no desire to tell you what you what I had. I also detest FB privacy policies. If friends or members of my family want to share something with me they can email me or send me a link. If they do not care enough about me to send me a link or email, I do not care enough to look at what they have to say or show. I have begun to use Google + a bit because I have better control over who sees what and can create 'circles' for real friends and family, a broader range of acquaintances and my even larger circle of 'business' contacts . As for Twitter, it's useful in an emergency such as our recent hurricane, but there is not much of value that can be imparted in 140 characters other than to point to a link
The funny thing is that I am not an old guy Luddite. I am working on the leading edge of cloud and big data text and data mining, but I have yet to drink the FB Kool-Aid because after looking at many FB posts I find little of interest or value in them, Of course I am more than happy to help my clients vacuum up all of that blather and create actionable market intelligence out of it or use it for eDiscovery, but since I know how it is used, I keep my distance from it.
Whether someone uses FB or is up to them but I do not understand some of the reasons. If it is because you don't care for what folks have for breakfast, where they are at the moment and with who, mudane political stuff, then it is really simple. DON'T FRIEND them. FB has many good use if you choose to use it. I think a lot of folks that do not use it actually have no clue how it works and the privacy settings that can be used.
I have no security issues using it, I only have friends that post relevent things in their lives, it is an easy way to keep in touch with family and friends. When my HS class was planning a reunion it was very helpful for the organizers.
People can't "see" what I am doing unless I let them. If folks are afraid of the government looking in they can do that with your emails just as easily as they can with FB.
Anyway, use it or not, just at least be educated in the privacy settings and what folks can and cannot see and how YOU contril who is your friends and family. (AdBlock kills all of the ads also so you don't get inundated with stuff, just like on DC!)
Then I heard the voice of the Lord saying, Whom shall I send? And who will go for us?
And I said, Here am I. Send me!
Isaiah 6:8
I have a theory that facebook and google will eventually become self-aware and turn into something like Skynet, but I still use them... I must be crazy.
"With your permission you give us more information about you, about your friends, and we can improve the quality of our searches [...] We don't need you to type at all. We know where you are. We know where you've been. We can more or less know what you're thinking about." - Eric Schmidt, CEO, Google.
I have no interest in, or use for, facetube.jpg or YouBook.JPG and I am not a Twit on tweeter.JPG so I MUST BE crazy!!!
An armed society is a polite society
Here is a list of all the reasons why I need a Facebook account:
...Oh wait, there are no reasons why I need a Facebook account.
You can follow me on Facebook...but you might not like where I'm going to take you
NRA Life Member
GOA Life Member
Behave Like Someone Who is Determined to be FREE!
He is no fool who gives what he cannot keep to gain what he cannot lose. - Jim Elliott
The world is a dangerous place to live; not because of the people who are evil, but because of the people who don't do anything about it.
Albert Einstein
I don't do facebook, utube, tweet, twit, or text. The only forum I'm a member of is this one. Guess I must be socially maladjusted. Oh, wait, maybe I'm just an old fart who doesn't think everything I do every moment of the day is of interest to someone else! However, I can see it's usefulness for someone in the military stationed away from their loved ones, etc.
Live to ride, ride to live. Harley Road King And keep a .45 handy Kimber Custom TLE II
If the Union is once severed, the line of separation will grow wider and wider, and the controversies which are now debated and settled in the halls of legislation will then be tried in fields of battle and determined by the sword.
Andrew Jackson
I use email for certain photos and information and FB for others. I carved a pumpkin the other night and it came out cool so I posted it on FB (only "Friends" can see your stuff).
Yeah, I could log onto my email, get a email composed, see if there is a specific group of emails already setup for sending something like that or create a group or selectively check on the emails of people that I want to send it too.
Or I can "click" take the picture on my phone, hit the little button which says to post to FB and it is done.
Now, which is easier in that situation? BTW: I just did it...took about 8 seconds for everybody to see.
It is convenience. Ya know, this thread is sort of like "who carries one in the chamber". I don't know why folks give a hoot how a carry (I do carry one in the chamber ) or how I post things on FB. Folks have different ways of doing things that suit their individual lifestyle and comfort level.
Then I heard the voice of the Lord saying, Whom shall I send? And who will go for us?
And I said, Here am I. Send me!
Isaiah 6:8
I was just puzzled by the earlier statement that you wouldn't have been able to get the pic
if not for FB. If FB made it more convenient for your kids to send pics of the grandkids, then
that is fine by me. No point to doing extra work and taking extra time if you don't have to.
Since I have never tried FB, I had no idea that advantage existed.
If the Union is once severed, the line of separation will grow wider and wider, and the controversies which are now debated and settled in the halls of legislation will then be tried in fields of battle and determined by the sword.
Andrew Jackson
'If youre of a certain age and you meet someone who you are about to go to bed with, and that person doesnt have a Facebook page, you may be getting a false name. It could be some kind of red flag,' he says.
If you decide to go to bed with someone based on a Facebook page...... you are a fool!
"A man's got to know his limitations." Inspector Harry Callahan


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What is CTECC?
The Career and Technical Education Curriculum Consortium (CTECC) is a web-based curriculum program initiated in 1998 by the Association of Career and Technical Education Administrators (ACTEA). CTECC has recently transitioned to Atlas Curriculum Mapping Software System. This web-based software allows similar program educators, such as automotive technology teachers, to establish learning communities and share best practices. Curriculum mapping allows teachers to identify gaps, redundancies and misalignments in the curriculum. This approach fosters dialogue among teachers that leads to increased measurable results in student achievement. An online tutorial option with an overview of the site and its functions is available and useful for local staff development.
Applications of CTECC
Instructions for CTECC Access
Welcome to the ACTEA curriculum system delivered via Atlas. It allows you to view the ACTEA CTE programs and communicate with instructors across New York. Follow these steps to get started:
For further information or to subscribe, contact Rubicon/Atlas at 1-800-845-3600 or Cathy Chamberlin at 716-628-0618 (cell) or email.


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by Ricker Polsdorfer, MD
ATTN: National Call Center
1701 North Beauregard ST
Alexandria, VA 22311
An important part of diabetes management is caring for your feet. Here, you'll find consumer-friendly information on foot-related concerns for people with diabetes.
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This site provides information related to foot care. It also includes links to other foot care organizations.
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This site provides consumer information on foot concerns and names of podiatrists in local areas.
Please be aware that this information is provided to supplement the care provided by your physician. It is neither intended nor implied to be a substitute for professional medical advice. CALL YOUR HEALTHCARE PROVIDER IMMEDIATELY IF YOU THINK YOU MAY HAVE A MEDICAL EMERGENCY. Always seek the advice of your physician or other qualified health provider prior to starting any new treatment or with any questions you may have regarding a medical condition.
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Appliance repair experts who've earned top ratings from Angie's List members offer advice for what it takes to keep your kitchen appliances in good condition.
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As stated above, it can vary between companies.
Typically just an inspection implies you do not have a contract or agreement that may include discounts or free repairs.
With our company you would get the annual maintenace service that you should do every year, and if repairs are needed, they are extra, but you aviod paying a "service call charge" that would be related to most repairs, because you are paying for the "inspection" and we are already on site.
Inspections are often discounted in the slow seasons, and can usually be found advertised , at reduced prices , on Angie's List.
So consider Angie's List and find the best of the best in HVAC contractors!
I have never seen one of this type that does not exit the house. You would not want the grease dumping into your basement, even with a filter it will happen.
The greater part of your job will be carpentry as if there is a wall behind the stove a hole will have to be cut up through the basement into the wall up to the stove. Unless it is one of the stoves that allows for it to fit inside a cabinet below. To answer correctly most here would be a picture of where this project is being done. I have done motorized ones that extend up out of the counter when in use and then retract. Those exit through the cabinet and require the cook top is to the front of the counter and not a drop in one
As an added note these tend to be better as they do not pull the heat away from the stove top when in use as much as the ones flush with the stove. I have install quite a few and happen to have an Amana cook top with built in down draft and I have to shut it of to get water to boil on the back burners.
A carpenter will know what can be cut and what not in the basement, a sheet metal contractor should know as well but at the other end for the finish by the stove they might not. Most carpenters that do kitchens have installed the minimal amount of duct work for this. They just have to be carefull with the number of ellbows and the lenght of the duct.
Appliance Repair reviews in Chehalis
When I initially called, I was informed that if the control board was the problem, replacement would be covered by the manufacturer. Other companies did not mention this possibility.
Darik showed up as scheduled and spent about thirty minutes to determine that the problem was a plugged water valve rather than the suspected issues. He did not have a valve available, but called to confirm they had one in stock. He set up an appointment for the following day to return with the new valve and quoted a fixed price which included credit for the initial call. He arrived an time the second day and replaced the valve in about twenty minutes. He clearly knew what he was doing.
Price was competitive with other companies I called.
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Merrell Women's Proterra Vim Sport Hiking Shoes
Save $5.02 (5%)
Product Information:
Gear up for adventure in the Merrell® Women's Proterra Vim Sport hiking shoe. Lightweight Stratafuse™ fabric hugs feet for a glove-like fit as you trek across natural terrain, while a rough-and-tough PU midsole increases ground contact for ultimate outdoor performance. Diamond-cut lugs maximize traction, allowing you to push your adventures to new limits. The next time you're looking to explore, sport the Proterra hiking shoe.
- Stratafuse™ fabric upper provides a glove like fit for lightweight, natural movements
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- Minimal design PU midsole increases ground contact for ultimate control
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- Protective TPU arch rand and toe cap shield feet from obstacles on the trail
- 2.5 mm, reversed, diamond-cut lugs grip natural terrain
- Proterra Vim® outsole with Sticky Rubber maximizes traction on rugged outdoor surfaces
- Weight: 12 oz
- Style: J57258
- Merrell
Country of Origin: China
Web ID: 18581156
Customer Reviews:
Merrell Women's Proterra Vim Sport Hiking Shoes
Excellent Hiking Shoe!
I am an avid hiker and this shoe is PERFECT for the trails. They are comfortable enough to be in for strenuous, 10 mile hikes. I've never gotten blisters from them or any discomfort. The toe box is super roomy and the arch is in the perfect spot. They dry very quickly. I would recommend these shoes to anyone!
May 5, 2014
Very, very comfortable and great support
I always have trouble finding shoes that fit, are comfortable, and provide great support - and I finally found them . I have medium wide feet and these give me plenty of room in the toe area. Have had them for about a year and wear them every chance I get. I've done some walking for exercise and some short hikes and they are fantastic. Would purchase another pair - actually, I just did in another color!
March 18, 2014
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Wheatsheaf Networking
TodayMonthly networking hosted by Branston Adams, The Wheatsheaf Pub and new partner, Phyllis Tuckwell Hospice.
Business Biscotti Networking Farnham
TodayRelaxed and popular networking group helping local business to connect.
Emmanuel Cooper Memorial Lecture 2015
05/03/2015318 Ceramics invite you to join them, and special guest Alison Britton OBE for the second in the series of the Emmanuel Cooper Memorial Lectures.
Jo Jammer's Chicago Blues Revue
05/03/2015Boogaloo Promotions: Jo Jammer's Chicago Blues Revue at the Farnham Maltings
Blood Donation Sessions
09/03/2015Generally healthy? Aged 17 or over? Then do something amazing and Give Blood.
Farnham Independent Networking
10/03/2015Based in Farnham in Surrey, Farnham Independent Networking meet every Tuesday Morning for Breakfast and Networking, where business connections are made.
Farnham Business Connections Lunchtime Networking Event
12/03/2015If you are a local business and looking to make more contacts join us for lunch Farnham Business Connections - A Business Networking group to suit everyone.
Messy Church @ Hale MC
14/03/2015Join us at Messy Church- make something for Mum, meet new friends, enjoy some food & have fun!
Mothers Day Lunch
15/03/2015Treat Mum to a fabulous 3 course meal at the Legacy Farnham Hog's Back Hotel – the kids will even be entertained!


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Apple iMac 27in 3.2GHz review
3.2GHz Intel Core i3-550, 4GB RAM, 27in 2560x1440 display, MacOS X 10.6
Apple is famed for its stylish and well-built computers, and the company's latest 27in iMac is no exception. It hasn't changed much in appearance from the last model, but this isn't a bad thing.
The 27in screen immediately catches your eye due to its sheer size. It has a huge resolution of 2,560x1,440 pixels, which is roughly equivalent to four 1,280x800 MacBook displays stuck together. It's great for tasks such as working in multiple documents side-by-side or using applications with lots of palettes such as Photoshop. The screen is also very bright, with wide viewing angles and accurate colours. Despite its size, it's easy to tilt or swivel the display single-handed for a more comfortable viewing position.
There's a Mini DisplayPort for connecting another monitor or a high definition TV, but you'll almost certainly need to buy an adapter since screens with Mini DisplayPorts aren't very common. Another device with a Mini DisplayPort output, such as a MacBook, can use the iMac's huge screen as a display, but this requires yet another adapter.
The iMac is equipped with a 3.2GHz Core i3 550 processor and 4GB of RAM. It's by no means slow, scoring 111 overall in our demanding Windows benchmarks, but we'd expect to see an even faster Core i5 processor in a computer at this price. The ATI Radeon 5670 graphics chip has 512MB of dedicated memory. It's powerful enough to play most 3D games, but will struggle with the very latest, most graphically-intensive titles. In Call of Duty 4 it scored a smooth 28.3fps, but only managed 14fps in Crysis. A model with an even faster i5 quad core processor and Radeon HD 5750 graphics card is available, but it costs £250 more.
The aluminium rear of the iMac became very warm when running our demanding benchmarks. It stayed almost silent though, which is impressive, so it won't sound intrusive in a quiet office.
If the 1TB hard disk isn't big enough for your needs, you'll need to add a USB2 or FireWire 800 hard disk, as the internal disk can't be accessed without disassembling the entire computer using specialist tools. Annoyingly, all of the ports are located on the rear of the iMac, so you have to swivel the computer around to access them. Only the DVD writer and SDXC memory card slot are located on the easier-to-reach right hand side.
It's a shame there isn't an internal Blu-ray drive, or even an option to add one – Apple would no doubt rather sell you HD movies through its iTunes Store. The built-in stereo speakers are surprisingly loud, although they sound muddier than we'd like. Thankfully, the headphone jack doubles as an optical S/PDIF connector for connecting a surround sound amplifier.
We were taken with the iMac's generally elegant design and superb, high quality screen. However, we found the slightly stingy choice of graphics card and processor annoying, as is the lack of a Blu-ray drive. If you can live with these limitations, and can afford it, the iMac is nonetheless a great all-in-one computer.


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Set your phone to see if this item is compatible.
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For all other issues, please go to support.ovi.com


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Hang tight!
Recipe by Retta
"Very nice with crab cakes, or chicken. basmati rice is best for this recipe."
Hmm. None of these ingredients are on sale today.
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2 tablespoons butter, divided
1 cup Basmati rice
2 cups water
2 cups fresh corn kernels
3 large shallots, sliced thinly
1/2 teaspoon white sugar
salt to taste
ground black pepper to taste
2 tablespoons chopped fresh mint leaves
This is a really good base recipe that can be made great! I cooked the rice in 1 cup organic, free range, low sodium chicken broth and 1 cup light coconut milk. I used canned corn and added some finely diced red pepper. I thought 3 shallots was a bit much, I used only one large one and served it with herb and garlic marinated grilled chicken cutlets. This made way more than 5 servings! I think this would be a great way to make couscous. You could even add cooked chicken or tofu to the mixture and serve it as a main course. Might be nice to sprinkle a little fresh lemon juice over the top just before serving as well. Thanks for a great base recipe!
this just tasted weird to me and bf agreed but said "weird in a good way".. i DID use dried mint so maybe that's why but i didn't think it was going to make that much of a difference.. this tasted "floral" to me.. splitting the difference, i'm giving it a 3 until i can get a hold of some fresh mint
45 Ratings
Even though this recipe looks like it might taste bland, the peppermint adds an unexpected subtle flavor that makes it taste anything but bland.
yummy! I always make short grain sticky rice, but i needed a change for an indian dish. This was very tastey! I didn't use any mint, however, because that just didn't sound appealing to me AT ALL. I used frozen corn because we had in in the freezer. Yum!
All of my favorite ingredients in one dish. I loved this one. Thanks for a GREAT recipe! The idea of the mint is awesome.
I always use Jasmine rice for every rice dish. This is very fresh tasting and tasty. I'm a Personal Chef and I make it for my clients.
This was a quick and easy side dish. I used brown rice instead of white and since I don't care for mint in savory dishes, I used fresh parsley instead. I also added some garlic. Thanks so much for the recipe!
I have to give 4 stars instead of 5 only because I didn't follow all of the recipe. I like to use what I have on hand, so I used a can of mexicorn instead of fresh corn, onion powder instead of shallots, and I didn't use any mint. But my family really enjoyed it so I will make it again the same way, since I usually have those ingredients on hand. However, I will probably decrease the butter just a tad.
* Percent Daily Values are based on a 2,000 calorie diet.
Corn and Rice Medley
Serving Size: 1/5 of a recipe Servings Per Recipe: 5 Amount Per Serving ** Calories: 263 ** Calories from Fat: 53
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Orientation activities get students involved early
By MOLLY WALTER
The Hays Daily News
The first six weeks of school at Fort Hays State University not only kick off with classes but also with Augustfest. It incorporates everything from freshman orientation to Tiger Impact. Augustfest is a cluster of events, social activities and ways for students to get involved on and connected to campus.
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By MOLLY WALTER
The Hays Daily News
The first six weeks of school at Fort Hays State University not only kick off with classes but also with Augustfest. It incorporates everything from freshman orientation to Tiger Impact. Augustfest is a cluster of events, social activities and ways for students to get involved on and connected to campus.
The first main event is PlayFair, which is Thursday at Lewis Field. PlayFair is one giant icebreaker required for freshmen and open to returning students.
"It's one of those events that with the right attitude, it's a great opportunity to meet a ton of people," said coordinator Shana Meyer, assistant vice president for Student Affairs.
Last year, more than 800 people attended PlayFair.
"It's almost chilling -- gives you goosebumps to see all that spirit and activity and the connections students are making," Meyer said.
Another big event is orientation, which also is required for freshmen. Its purpose is for freshmen to learn about the changes and transitions students will face in college.
The university brings in a keynote speaker, and this year the speaker is Kyle Cease, one of Comedy Central's top upcoming comedians. Cease performed hundreds of college shows and suddenly got debilitating stage fright, so he reassessed his life and now does comedy talks about doing what makes you happy and how to handle stress and change.
"I think he'll be really funny and have a really good message as well," Meyer said.
Cease also will be doing a comedy show Friday for the public.
A newer event on the Augustfest schedule will be Aug. 19. This is only the second year of the Social Excellence Program, where students learn to come out of their shells and what's expected of them in college.
"They learn that who they were in high school isn't who they have to be in college. So it's kind of like a networking type opportunity and a challenge to students at the same time," Meyer said.
The largest event anyone can attend is the Back to School Picnic, where student organizations set up booths and get their names out to new and returning students.
"It's open to the community, all students, faculty and staff. Everyone gets involved in that," Meyer said.
Adult Learner Orientation is a smaller event but is important for students who are coming back to school for the first time -- whether they've been gone two or 20 years. It includes information from library orientation to technology orientation.
Other events during Augustfest are put on by several other campus organizations including Intramurals, sorority and fraternity recruitment, Christian Challenge, University Activities Board and Residence Hall Association. Academic departments also host department gatherings.
"One of the big goals of it is even if there's a social activity, there are goals behind that activity. So we're trying to really get the students engaged with each other, start forming connections not only with their peers but also with services on campus and resources on campus. It's all really part of an overall retention effort to get students involved on campus," Meyer said.


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Play Slideshow >>
Power Parasol Lot 59, by Debartolo Architects
View beneath the solar roof.
Michael Nothum
Panelized roof.
View north.
Site plan.
Courtesy De Bartolo Architects
Structure and panels exploded axonometric diagram.
View of panels from below.
Power Parasol beside the football stadium.
Parking structure in use.
The structures also serve as event spaces, with supporting elements also used for signage.
Panel installation.
C-channel connections.
Sunset between the structures.
Category: Move Honorable Mention
Part civic shade structure, part energy generator, and part billboard, Power Parasol Lot 59 is a galvanized steel structure topped by 7,600 photovoltaic panels that covers an existing parking lot for 800 vehicles at Arizona State University's Tempe, Ariz., campus. Designed by Phoenix-based Debartolo Architects, who worked in concert with a team of structural and electrical engineers, the 227,700-square-foot canopy generates over 2.2 megawatts of electricity. It is supported by slender columns that provide the supporting armature for hanging banners, advertisements, and lighting.
"It's a 5-acre project, so I'm thinking about the colossal scale of this, but then there's this level of refinement in the assembly with which I was really impressed." —Elizabeth Ranieri
Project Credits
Project Power Parasol Lot 59, Phoenix Owner NRG Solar—Thomas Reagan Host Arizona State University, Tempe Campus Developer Strategic Solar Energy Architect Debartolo Architects, Phoenix—Jack DeBartolo III, AIA Contractor Hardison/Downey Construction—Kevin Vander Molen, AIA Structural Engineer Rudow + Berry—Mark Rudow Electrical Engineer Taylor Rymar Corp.—Dan Simpson Civil Engineer Evans Kuhn & Associates—George Evans Landscape Engineer JJR Floor—Kris Floor Geotech Consultant Speedie & Associates Size 227,700 square feet Cost Withheld Photographer Michael Nothum
Sponsored EDUCATION
Renewable Energy
Solar Power
Transportation Projects
Phoenix-Mesa-Scottsdale, AZ
Katie Gerfen
Annual Design Review
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