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134 Merton Street, Boggabri NSW 2382 - Ph: (02) 6743 4322 - Fx: (02) 6743 4245
Situated just 3kms From Town Centre, this property has a 3 bedroom elevated home with lovely rural views. Features 2 sunrooms, excellent kitchen, neat bathroom and enclosed house yard. The acreage offers 1 equipped windmill, 1 dam, wooden cattle yards, sundry sheds. 20m x 30m corrugated iron shed. VENDORS ARE KEEN SELLERS AND WILL NEGOTIATE ON PRICE
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Gear review: Revo Heading sunglasses offer versatile protection
When you're trying to pack light, it becomes impossible to bring along sunglasses for each endeavor: on the water, off the water, for sports, for glamour. Better to have one pair that looks good and is tough enough for all your travel adventures, to boot. The Revo Heading sunglasses have high-contrast polarized Serilium lenses, and a sturdy frame with plenty of color options to fit your style. The frames have a spring hinge, which allows a greater range of motion and helps with durability, so they'll last longer unless you sit on them or leave them on the plane. An elastomeric nose pad keeps the shades on your face when you're active, or just actively sweating on a bar stool in the tropical heat of some exotic destination.
What we liked: Revo's polarized lenses are sheer rock stars for blocking 100 percent of UVA, UVB and UVC light, as well as absorbing visible light - protecting your eyes whether you're on land or water.
Not so much: Those who want more full coverage in a frame might look to Revo's Bearing shades for bigger faces.
Vitals: $189 from revo.com.

subset: commoncrawl


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After doing some yard work in the middle of the landlocked world, I went through my emails and saw where I wanted to be: Panama. A press release reminded me that the ISA (International Surfing Association) world championship event was wrapping up near Santa Catalina, Panama. I tuned in, mirrored my computer to the Apple TV in the living room, and watched men and women from all over the world finish the team surf competition. It was a terrific visual event – extremely well-produced – and if you've never been to a surf contest, it captured the patience, power and passion required to succeed in this sport. I had the chance to cover many tournaments and pro surfing events in my career while living in California.
The women's individual world champ comes from Australia, Dimity Stoyle. Claiming the men's championship, from South Africa, Shaoun Joubert. But this is a team contest – and the coveted 2013 Reef ISA World Surfing Games team title…
9th place Venezuela
8th Chile
7th Argentina
6th Costa Rica
5th Panama
4th Brazil
3rd Peru
2nd Australia
and the champs are…
South Africa
I've been out of the surfing contest loop for some time, so I have no idea why the US and Hawaii, France and Portugal aren't there (had to be politics, at least in the world of surf politics!)… The contest was still a blast to watch and you should check it out on replay on their website.
I think I need to grab my board and head towards the gulf this summer – the closest waves I can find!


text: Most people's diets are woefully inadequate for providing proper nutrition. Even good diets fail to deliver sufficient levels of nutrients. The Vitamin Cure book series highlights the safe and clinically effective use of vitamin supplements for a variety of illnesses. Research continues to prove the immense value of vitamins for maintaining health and fighting disease. The Vitamin Cure books, written by authors who are recognized experts in their field, deliver authoritative, up-to-date, and practical information on taking vitamins for particular health problems. There is an epidemic of diabetes and the problem is only getting worse. More than 220 million people worldwide have diabetes, and over 3 million people die from the consequences of the disease each year. Diabetes deaths will double by the year 2030. Diabetes mellitus affects the use of sugar (glucose) in the body, either because the body does not produce enough insulin or the cells do not respond to it. High levels of blood glucose become toxic to many tissues and organs and may result in blindness, kidney failure, brain and nerve damage, heart disease, and rapidly developing atherosclerosis. Fortunately, there is an answer. The Vitamin Cure for Diabetes can help the majority of diabetics come off all or most medications by changing their lifestyle, eating a healthier diet, starting to exercise, and taking nutraceuticals. This book provides a complete supplement program (vitamins, minerals, and other dietary supplements) that can prevent or delay the onset of diabetes. Readers will learn how to optimally manage, or even prevent, diabetes for themselves and for their loved ones.


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My Dear Friends and Followers,
When we last met it was Christmas Eve and almost two months gone...
The beginning of 2015 was extra busy for us. Emma, Charles and I moved to another flat which we love very much but still have a lot to do. Our furniture and other stuffs are still in boxes (we can't even find many things) and have to build our new life.
We plan to buy new furniture for our kitchen (it will be more modern and beautiful, You'll see it next month!), new wallpaper for all of the rooms and a big bed for the sweetest dreams!
We will try to inform You regularly, and until we can meet again, please, visit Rosemary's other blog: (Ever After) Rozmaring. (It was written in Hungarian but You can find a translator at the top on the right.) She wrote the first chapter one year ago and never continued till yesterday, when a new doll arrived home... We both hope You will enjoy it.
Have a nice Sunday and see You next month!
Lots of love:


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Premiere Exclusive
Danielle Strickland
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Danielle Strickland
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Danielle Strickland is currently based in Toronto, Canada. Her aggressive compassion has served people firsthand in countries all over the world. From establishing Justice Departments for The Salvation Army to launching Global anti-trafficking initiatives, to creating new movements to mobilize people towards transformational living. Danielle trains, advocates, and inspires people to live differently.
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A Boundless Life
How do we live out a faith that is rich and free, deep and wide? How does our personal faith journey become something that effects change in the world? Practicing a faith that keeps Je- sus ...
4 steps to Freedom
How to fight against oppression and live in freedom through Jesus. Everyone can feel the im- pact that oppression can leave on your daily life. An erosion of hope, a weariness of heart, a ...
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One of the first revelations of God was a way of re-framing absolutely everyone and everything with a sacred lense. What Jesus invites us to live is a life that follows His example. What ...


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In melanocytes and melanoma cells, cAMP activates extracellular signal‐regulated kinases (ERKs) and MEK‐1 by an unknown mechanism. We demonstrate that B‐Raf is activated by cAMP in melanocytes. A dominant‐negative mutant of B‐Raf, but not of Raf‐1, blocked the cAMP‐induced activation of ERK, indicating that B‐Raf is the MEK‐1 upstream regulator mediating this cAMP effect. Studies using Clostridium sordelii lethal toxin and Clostridium difficile toxin B have suggested that Rap‐1 or Ras might transduce cAMP action. We show that Ras, but not Rap‐1, is activated cell‐specifically and mediates the cAMP‐dependent activation of ERKs, while Rap‐1 is not involved in this process in melanocytes. Our results suggest a novel, cell‐specific mechanism involving Ras small GTPase and B‐Raf kinase as mediators of ERK activation by cAMP. Also, in melanocytes, Ras or ERK activation by cAMP is not mediated through protein kinase A activation. Neither the Ras exchange factor, Son of sevenless (SOS), nor the cAMP‐responsive Rap‐1 exchange factor, Epac, participate in the cAMP‐dependent activation of Ras. These findings suggest the existence of a melanocyte‐specific Ras exchange factor directly regulated by cAMP.
Melanocytes are neural crest‐derived skin cells specialized in the synthesis of melanin pigments. This process is regulated by a physical stimulus such as ultraviolet (UV) A/B radiation or hormonal stimuli evoked by pro‐opiomelanocortin hormones like α‐melanocyte stimulating hormone (α‐MSH). α‐MSH, by binding to the melanocortin 1 receptor (MC1‐R) on melanocytes and up‐regulating the cAMP pathway, induces melanocyte and melanoma cell differentiation (Levine et al., 1991). This process is characterized by increased melanin synthesis (Hearing and Jimenez, 1989; Hearing and Tsukamoto, 1991) and dendrite outgrowth crucial for pigment delivery within the epidermis (Buscà et al., 1996, 1998). In previous studies undertaken to characterize the molecular events triggered by cAMP during melanocyte differentiation, we have shown that the elevation of intracellular cAMP provokes the activation of the mitogen‐activated protein kinase (MAP kinase, or MAPK) ERK1 in B16 mouse melanoma cells (Englaro et al., 1995).
ERK1 and ERK2 are serine/threonine protein kinases activated upon dual phosphorylation by the MAPK kinase (MAPKK) MEK (reviewed in Robinson and Cobb, 1997), which in its turn is phosphorylated and therefore activated by the MAPKK kinases of the Raf family (Moodie et al., 1993). Raf kinases are activated after their interaction with the GTP‐bound form of p21Ras (reviewed in Morrison and Cutler, 1997), and the levels of Ras–GTP are mainly controlled by Ras‐specific guanine nucleotide exchange factors such as Son of sevenless (SOS) or R‐Ras–GRF. When activated, ERKs translocate to the nucleus where they regulate gene expression, leading to cell proliferation or differentiation depending on the cell type. Interestingly, the activation of ERKs by cAMP has been reported in a limited number of cell systems, including B16 melanoma cells and PC12 phaeochromocytoma cells (Frodin et al., 1994; Young et al., 1994; Englaro et al., 1995) which are also derived from the neural crest. Several other studies have tried to determine the mechanism of ERK activation by cAMP in PC12 cells. Vossler et al. (1997) have shown that agents that increase the intracellular cAMP content, through protein kinase A (PKA) and the sequential activation of Rap‐1 small GTPase and B‐Raf kinase, activate ERK in a Ras‐independent manner.
The Raf family of kinases is composed of the ubiquitously expressed Raf‐1 and by A‐Raf and B‐Raf. B‐Raf, which is highly present in neural cells and tissues (Marx et al., 1988; Eychene et al., 1992; Barnier et al., 1995), lies downstream of Ras and upstream of MEK during nerve growth factor (NGF)‐induced signal transduction in PC12 cells. B‐Raf appears to be the major MAPKK activated in these cells after stimulation by NGF (Troppmair et al., 1992; Jaiswal et al., 1994; Lange‐Carter and Johnson, 1994; Traverse and Cohen, 1994). It is also the major MEK activator in bovine brain (Catling et al., 1994).
Rap‐1 is a member of the Ras superfamily of small GTP‐binding proteins. It has an effector domain almost identical to that of Ras, indicating that both small GTPases might share common downstream effectors. Rap‐1 can be activated by several second messengers like calcium and diacylglycerol (McLeod et al., 1998; Zwartkruis et al., 1998), and by cAMP, since Rap‐1 is phosphorylated by PKA (Lerosey et al., 1991) and this seems to participate to the Rap‐1 GTP loading (Altschuler et al., 1995). The physiological role of Rap‐1 remains to be elucidated. It has been suggested that Rap‐1 could antagonize Ras‐dependent signalling (Cook et al., 1993; Hu et al., 1997, 1999), but the recent work of Zwartkruis et al. (1998) does not support this notion. Recent studies have reported the cloning of different nucleotide exchange factors for Rap‐1 [Epac (also named cAMP‐GEFI) and cAMP‐GEFII) directly activated by cAMP (De Rooij et al., 1998; Kawasaki et al., 1998). This finding has revealed that, in addition to a PKA‐dependent regulation of Rap‐1, the activity of the small GTPase can be controlled by cAMP in a PKA‐independent manner.
In B16 melanoma cells, we have previously shown that cAMP activates MEK but fails to activate Raf‐1. In an attempt to identify the molecular events connecting cAMP to ERK activation in melanocytes, we examined the involvement of Rap‐1 and B‐Raf in the cAMP‐induced activation of ERKs in human melanocytes and in B16 mouse melanoma cells. Our results demonstrate that cAMP can activate Rap‐1 and B‐Raf kinase, but only B‐Raf mediates the cAMP effects on ERK activation. cAMP activated the Ras small GTP‐binding protein by a mechanism that involves neither PKA nor the exchange factors SOS or Epac. Finally, the activation of ERK by cAMP was blocked by a dominant‐negative mutant of Ras, demonstrating that Ras mediates the action of cAMP. Our results reveal novel mechanism of MAPK pathway activation by cAMP involving Ras and B‐Raf as signalling molecules.
cAMP activates MAPKs and B‐Raf in melanocytes
We have previously shown that, in B16 mouse melanoma cells, agents that increase cAMP concentrations activate the ERK1 MAPK (Englaro et al., 1995). Using specific antibodies against the phosphorylated, and thus activated, forms of ERKs or MEK‐1, we show here that cAMP‐elevating agents, isobutylmethylxanthine (IBMX) plus forskolin or α‐MSH, rapidly (within 5–10 min) activate ERK1, ERK2 and MEK (Figure 1A and B). ERK activation by cAMP also occurred in normal human melanocytes, which constitute a more physiological system (Figure 1A). In contrast, cAMP‐elevating agents did not activate ERKs in NIH 3T3 mouse fibroblasts (Figure 1A). 12‐O‐tetradecanoyl phorbol‐13‐acetate (TPA) was used in all cases as a positive control, since it strongly activates ERKs. Thus, MAPK activation by cAMP seems to be a tissue‐specific process, which takes place in melanocyte cells.
In an attempt to discover the precise mechanisms leading to MEK and ERK activation by cAMP in melanocyte cells, we measured Raf‐1 and B‐Raf activities upon cAMP treatment of B16 melanoma cells. Raf‐1 was not activated by cAMP in B16 cells, as has been described previously (Englaro et al., 1995). TPA strongly activated Raf‐1, but the pretreatment of cells with cAMP‐elevating agents markedly impaired the TPA‐induced Raf‐1 activity (Figure 1C). In contrast, B‐Raf immunokinase assays showed that the cAMP‐elevating agents (IBMX plus forskolin, or α‐MSH), as well as TPA, used as a positive control, significantly activated the kinase (Figure 1C). These results suggest that B‐Raf, but not Raf‐1, mediates the cAMP‐stimulation of MEK and ERKs in B16 cells.
B‐Raf is the MAPKKK that transduces the cAMP activation of ERKs in B16 melanoma cells
To verify this hypothesis, haemagglutinin‐tagged ERK1 (HA–ERK1) was cotransfected with epitope‐tagged dominant‐negative mutants of B‐Raf or Raf‐1 or with constitutive active mutants of the kinases. Then, after treatment with cAMP‐elevating agents and immunoprecipitation of the tagged ERK1, we evaluated ERK activation by western blot experiments using an antibody specific to the phosphorylated (active) ERKs. ERK1 phosphorylation was greatly increased by the overexpression of constitutive active mutants of both B‐Raf and Raf‐1 (Figure 2A). As expected, cAMP‐elevating agents activated HA–ERK1 in B16 cells. This activation was blocked by the dominant‐negative mutant of B‐Raf but not by the dominant‐negative mutant of Raf‐1, indicating that the cAMP activation of ERKs follows the B‐Raf 'sub‐pathway'.
The Raf‐1 dominant‐negative function was verified in Chinese hamster ovary (CHO) cells, in which Raf‐1 is the predominantly expressed MAPKKK (not shown). As expected, N‐Raf‐1 blocked the TPA‐activated ERK activity (Figure 2B). The level of the transfected protein expression was verified by western blot analysis using the anti‐tag antibody (Figure 2A and B, lower panels).
Rap‐1 and Ras are putative upstream B‐Raf activators mediating the cAMP stimulation of ERKs
As an approach to identifying the upstream activators of B‐Raf likely to mediate cAMP stimulation of ERKs, we investigated the role of small GTP‐binding proteins of the Ras family by using Clostridium sordelii lethal toxin (LT) or Clostridium difficile toxin B. LT acts specifically by inhibiting the small GTPases Ras, Rap‐1 and Rac (Just et al., 1996; Popoff et al., 1996) and toxin B specifically inhibits the Rho family of small GTPases Rho, Rac and CDC42 (Just et al., 1995; Chaves‐Olarte et al., 1996). In our hands, low concentrations of LT (70 ng/ml) completely inhibited the cAMP‐induced activation of MAPK (Figure 3), suggesting that Ras, Rap‐1 or Rac mediated the action of cAMP. On the other hand, toxin B did not affect the cAMP‐induced ERK activation (Figure 3), indicating that the small GTPases of the Rho family, including Rac, do not play a significant role in this process in melanocytes.
We have previously reported that the inhibition of Rho‐family proteins by toxin B induced disruption of stress fibres, leading to characteristic morphological alterations in B16 cells (Buscà et al., 1998). Toxin B action was therefore verified by examining cells by phase‐contrast microscopy (not shown). Taken together, these results suggest that Ras and Rap‐1 may mediate the activation of MAPK by cAMP in B16 cells.
cAMP activates Ras and Rap‐1
Next, pull‐down experiments were carried out to measure the effect of cAMP on Ras and Rap‐1 activities. To detect activated Ras, we used a glutathione S‐transferase (GST) fusion protein containing the B‐Raf Ras‐binding domain (B‐Raf RBD); to detect activated Rap‐1, we used a Ral–GDS RBD (RGF–RBD) fusion protein (Herrmann et al., 1996).
Cells were treated with IBMX and forskolin or with α‐MSH to increase cellular cAMP levels, and cell lysates were incubated with each GST fusion protein coupled to glutathione–Sepharose beads. The bound proteins were analysed by western blotting to detect Ras or Rap‐1. Rap‐1 binding to the RGF–RBD was increased upon treatment with cAMP‐elevating agents in both B16 melanoma cells and in NIH 3T3 cells, indicating that Rap‐1 is activated by cAMP in these cell lines (Figure 4A). In B16 cells exposed to cAMP‐elevating agents, Ras binding to the B‐Raf RBD was strongly stimulated, so cAMP can also activate Ras (Figure 4B). We also detected significant Ras activation by cAMP in normal human melanocytes, thus giving a more physiological relevance to our observation (Figure 4B). Conversely, in NIH 3T3 cells, cAMP did not activate Ras while platelet‐derived growth factor (PDGF), used as a positive control, clearly increased the binding of Ras to B‐Raf RBD (Figure 4B).
Taken together, these results show that Rap‐1 is activated by cAMP in both B16 melanoma cells and NIH 3T3 cells. However, Ras, which is specifically activated by cAMP in melanocytes but not in NIH 3T3 fibroblasts, fulfils the conditions required to transduce the cAMP‐induced stimulation of ERK in a cell‐specific manner.
Ras but not Rap‐1 mediates the cAMP‐activation of ERKs in B16 melanoma cells
To analyse directly whether Rap‐1 or Ras mediated the cAMP‐induced stimulation of MAPK in B16 melanoma cells, we investigated ERK activation by cAMP in cells expressing dominant‐negative (HA–Rap‐1‐N17 or HA–Ras‐N17) or constitutive active mutants (HA–Rap‐1‐V12 or HA–Rap‐1‐E63, or HA–Ras‐V12) of both small GTPases (Figure 5). Cells cotransfected with these constructs and the HA‐tagged ERK1 were treated or not with cAMP‐elevating agents and the HA–ERK1 was immunoprecipitated with an anti‐HA antibody. The activated ERK was then detected by western blotting using an antibody against the phosphorylated forms of ERK. As shown in Figure 5, overexpression of the constitutively active Ras greatly increased ERK activation whereas overexpression of two constitutively active forms of Rap‐1 (Rap‐1‐V12 and Rap‐1‐E63) did not affect the activation state of the kinase. Only the dominant‐negative mutant of Ras, and not that of Rap‐1, completely blocked the cAMP‐induced ERK activation. The level of expression of the transfected protein expression was verified by western blotting with an anti‐HA antibody (Figure 5A, lower panels). Pull‐down experiments after overexpression of Rap‐1‐V12 and Rap‐1‐E63 confirmed that these mutants were constitutively active (Figure 5B).
Taken together, these results demonstrate that Ras mediates the activation of ERK by cAMP in B16 melanoma cells, whereas Rap‐1 does not seem to play a significant role in the activation of the MAPK cascade in this cell system.
cAMP activation of Ras/ERK is PKA‐independent
Most of the cellular effects of cAMP have been attributed to the activation of the cAMP‐dependent protein kinase (PKA). To determine whether the activation of Ras by cAMP in melanocyte cells was PKA‐dependent, we incubated B16 cells with H89, a potent and selective inhibitor of PKA. Figure 6 shows that H89, which inhibits PKA activity in B16 cells at a concentration of 3 μM (Figure 6C) did not inhibit the cAMP activation of Ras (Figure 6A) or the cAMP‐dependent phosphorylation of ERK (Figure 6B). Overexpression of the catalytic subunit of PKA did not affect ERK activation either (Figure 6D). Control experiments to investigate the function of the transfected PKA catalytic domain were performed by cotransfecting this vector with a plasmid encoding the PKA‐responsive cAMP‐responsive element (CRE) sequence cloned upstream of the luciferase reporter gene. The PKA catalytic subunit strongly stimulated luciferase activity (not shown). These findings demonstrate that cAMP activates the MAPK pathway in a PKA‐independent way.
SOS and Epac do not participate in the cAMP‐dependent activation of the MAPK cascade in melanocytes
Next, we investigated the involvement of SOS, the classical guanine nucleotide exchange factor for Ras, in the cAMP‐activation of Ras. We blocked the SOS‐dependent regulation of Ras by using a dominant‐negative mutant of SOS (ΔSOS) which lacks amino acids 618–1036 corresponding to the guanine nucleotide exchange domain of the molecule. B16 melanoma cells were cotransfected with the HA‐tagged ERK1 plasmid and with an empty vector or the dominant‐negative version of the factor (ΔSOS). Next, cells were treated or not with cAMP‐elevating agents and ERK phosphorylation was examined. cAMP‐elevating agents activated ERK in cells transfected with an empty vector. The overexpression of ΔSOS did not impair this activation, so SOS does not constitute the Ras upstream molecule regulated by cAMP (Figure 7A). The levels of expression of the transfected protein were verified by western blotting with anti‐HA and anti‐SOS antibodies (Figure 7A, lower panels). We confirmed the dominant‐negative function of ΔSOS as this construct inhibited the insulin activation of ERK in CHO cells stably expressing the insulin receptor (Figure 7B).
As SOS is not involved in the cAMP‐induced cascade in melanoma cells, we assessed the putative involvement of Epac, a recently described exchange factor for Rap‐1, directly activated by cAMP. We performed the same experiment described above using a plasmid encoding an Epac protein lacking the cAMP‐binding domain (EpacΔcAMP) which represents an activated version of this exchange factor (De Rooij et al., 1998). EpacΔcAMP neither induced ERK activation nor influenced ERK activation by cAMP, showing that Epac is not involved in the cAMP response towards ERK in B16 melanocytes. The level of expression of the transfected protein was verified by western blotting using an anti‐HA antibody (Figure 7C, lower panel).
Ras is not involved in the activation of ERK by cAMP in PC12 cells
In PC12 cells, ERKs and B‐Raf are activated by cAMP (Vossler et al., 1997). The common embryonic origin of PC12 cells and melanocyte cells has prompted us to investigate whether Ras could be activated by cAMP in PC12 cells. We therefore performed some experiments in this neuronal cell model. We first looked at ERK activation. cAMP‐elevating agents, like TPA, strongly activated ERKs, as seen by western blotting with an anti‐phospho‐ERK antibody (Figure 8A). Next, pull‐down experiments were performed to measure Rap‐1 and Ras activation in PC12 cells. Rap‐1 was activated by cAMP‐elevating agents (Figure 8B), as reported by Vossler et al. (1997). In contrast, cAMP did not activate Ras in PC12 cells (Figure 8C). NGF was used as a positive control for Ras activation (Figure 8C).
Finally, we overexpressed HA‐tagged constitutively active mutants of Ras, Rap‐1 and both Raf isoforms, Raf‐1 and B‐Raf, together with HA–ERK1. As described before, HA–ERK was immunoprecipitated and a western blot using an antibody to the phosphorylated forms of ERKs was then performed. As expected, the active form of Ras (Ras‐V12), as well as both active mutants of Raf‐1 (Raf‐1‐CAAX) and B‐Raf (B‐Raf‐CAAX), activated ERK1 in PC12 cells. Surprisingly, the functional constitutively active mutant of Rap‐1, Rap‐1‐E63, induced no ERK activation in these cells (Figure 8D). The same result was obtained using the other constitutively active mutant of Rap‐1, Rap‐1‐V12 (not shown). The expression levels of the transfected proteins were verified by western blotting using an anti‐HA antibody (Figure 8D, lower panels). Identical results were obtained with PC12 cells from three different origins (see Materials and methods), excluding the possibility that our results were not specific to the PC12 cells used in our study.
Taken together, these data indicate that, although Rap‐1 is activated by cAMP, it does not transmit the cAMP effects on ERK in PC12 cells. They clearly show that Ras cannot mediate these effects either, since it is not activated by cAMP in this cell system. Thus, the activation of Ras by cAMP appears to be a highly specific process, so far only known to occur in melanocytes.
We have investigated the mechanism by which cAMP activates the MAPK(s) ERK(s) in melanocytes and melanoma cells. We found that B‐Raf mediates the cAMP‐activation of ERK in melanoma cells. We also observed that cAMP activates Rap‐1, but does not seem to participate in the regulation of ERK by cAMP. Unexpectedly, we found that p21Ras is activated by cAMP and transduces the cAMP‐dependent activation of ERK in melanoma cells. Ras activation occurs through a PKA‐independent process that involves neither SOS nor Epac. We detected ERK and Ras activation by cAMP in normal human melanocytes, further strengthening the physiological relevance of the results obtained in the B16 melanoma cell line.
To date, cAMP has been reported to stimulate ERK activity in a very limited number of cell types, including T cells (Saxena et al., 1999), PC12 rat phaeochromocytoma cells (Frodin et al., 1994; Young et al., 1994) and melanocytes (Englaro et al., 1995). In T cells, the effect of cAMP on ERKs is mediated through the inhibition of a protein tyrosine phosphatase (Saxena et al., 1999). In PC12 cells the effect of cAMP has been proposed to involve the phosphorylation and activation by PKA of Rap‐1 small GTPase, then Rap‐1 up‐regulates B‐Raf activity which in turn phosphorylates and stimulates MEK, resulting in ERK activation (Vossler et al., 1997). The fact that both PC12 cells and melanocytes derive from the neural crest has prompted us to hypothesize that they share cell‐specific signalling mechanisms responsible for this MAPK cascade activation. Indeed, our data and those reported in PC12 cells suggest that B‐Raf is a key component in the pathway leading to ERK activation by cAMP.
Next we wished to elucidate the mechanisms by which cAMP regulates B‐Raf activity. Experiments using bacterial toxins suggested that Rap‐1 and Ras might function upstream of B‐Raf. Indeed, cAMP activates Rap‐1 in B16 cells but we found that two different functional constitutively active mutants of Rap‐1 were not able to induce ERK activation. Furthermore, a dominant‐negative mutant of Rap‐1 which has been reported to block the function of the endogenous protein (Vossler et al., 1997; York et al., 1998) did not prevent the activation of ERK by cAMP. These observations indicate that Rap‐1 does not participate in the molecular events connecting cAMP to ERK in B16 cells.
Although Rap‐1 is activated by cAMP in melanocytes, the physiological role of this event remains to be elucidated. Melanocyte differentiation is characterized by increased melanin synthesis and distribution within the epidermis. Melanin is produced and transported within specialized vesicles called melanosomes. The localization of Rap‐1 in the vesicular/endocytic compartment (reviewed in Bos, 1998) is compatible with a putative role of Rap‐1 in melanosome dynamics. Bourneville's disease, or tuberous sclerosis complex (TSC), is an autosomal dominant syndrome characterized by the widespread development of hamartomas, mental retardation and a skin pigmentation disorder (Sheth, 1998). The product of the TSC2 gene is tuberin, which has a specific GTPase activity towards Rap‐1 (Geist et al., 1996; Wienecke et al., 1997). This observation, indicating that the alteration of Rap‐1 function is associated with a pigmentation defect, supports the hypothesis that Rap‐1 is involved in melanocyte differentiation.
The lack of Rap‐1 involvement in cAMP‐induced ERK activation in melanoma cells suggests that Ras could be the mediator in this process. This attractive hypothesis was confirmed by pull‐down experiments which demonstrated that cAMP activates Ras, as shown by its increased binding to the B‐Raf RBD. The fact that Ras activates the ERK pathway is well known (reviewed in Johnson and Vaillancourt, 1994), but our results disclose a novel mechanism in which Ras may act as an early transducer of the cAMP‐dependent activation of MAPK in melanocytes. It is well established that Ras–GTP activates both B‐Raf and Raf‐1. However, we show here that Raf‐1 is not activated by cAMP. Furthermore, cAMP inhibits Raf‐1 activation by TPA. Raf‐1 inhibition by cAMP has already been reported (Wu et al., 1993; Moodie et al., 1994; Vaillancourt et al., 1994) and seems to be mediated by Raf‐1 phosphorylation by PKA at Ser43 and Ser621 (Wu et al., 1993; Häfner et al., 1994; Mischak et al., 1996). B‐Raf is not inhibited by the up‐regulation of the cAMP pathway (Vossler et al., 1997; MacNicol and MacNicol, 1999). This was initially explained by the absence, in B‐Raf, of the PKA phosphorylation site homologous to Ser43 in Raf‐1. More recently, B‐Raf resistance to PKA was explained in a report demonstrating that the N‐terminal regulatory domain of B‐Raf interfered with the ability of PKA to phosphorylate the kinase and modulate its activity (MacNicol and MacNicol, 1999). Thus, it was tempting to propose that, upon the cAMP‐induced Ras activation, the concomitant activation of PKA led to the inhibition of Raf‐1, making B‐Raf the only MAPKKK involved in the activation of ERK by cAMP. However, this possibility has been ruled out because we have not been able to release the blockade of Raf‐1 activity upon cAMP treatment by the use of a PKA inhibitor (not shown). Thus we must conceive another hypothesis that could eventually involve (i) RKIP, a recently described inhibitor of Raf‐1 (Yeung et al., 1999), (ii) Akt (PKB), which inhibits Raf‐1 and is activated by cAMP (Zimmermann and Moelling, 1999; Scheid and Woodgett, 2000) or (iii) Rap‐1 itself, which has been reported to antagonize Ras‐dependent Raf‐1 activation in some cell systems (Cook et al., 1993; Hu et al., 1997, 1999).
Our data and those of Vossler et al. (1997) reveal that PC12 phaeochromocytoma cells and melanocytes share some specific signal transduction features, at least concerning the activation of ERK, MEK and B‐Raf by cAMP. However, our findings clearly demonstrate the existence of different regulatory mechanism since Ras is activated by cAMP in melanocytes but not in PC12 cells. Further, in melanocyte cells, two constitutively active Rap‐1 mutants were unable to activate ERK. In our hands, these mutants also failed to activate the MAPK pathway in PC12 cells. Our results are in total agreement with the data of Zwartkruis et al. (1998), demonstrating that, in PC12 cells, Rap‐1 activation does not correlate with ERK activation. Thus the activation of B‐Raf by Rap‐1 may be restricted to a very specific PC12 subclone (the PC12‐GR5 variant used by Vossler et al.) or to certain experimental conditions such as upon overexpression of both Rap‐1 and B‐Raf (Vossler et al., 1997; Okada et al., 1999).
In most cell systems, cAMP effects have been considered to be the result of PKA activation. However, cAMP interacts directly with some ion channels (Zufall et al., 1997; Santoro et al., 1998) and PKA has not been clearly implicated in the cAMP‐regulation of certain neural functions (Huang et al., 1995; Liu et al., 1995; Brandon et al., 1997). We have shown that, in B16 cells, the cAMP‐dependent activation of Ras, and therefore ERKs, is PKA‐independent. When thinking about possible cAMP‐dependent regulatory points for Ras, we focused our attention on SOS, the classical guanine nucleotide exchange factor that usually couples tyrosine kinase growth factor receptors to Ras activation (reviewed in Bar‐Sagi, 1994; Schlessinger, 1994). Since SOS recruitment to the plasma membrane is sufficient to activate Ras, cAMP, by some unknown mechanism, could target SOS to the membrane, thereby activating Ras. However, the overexpression of a dominant‐negative mutant of SOS (ΔSOS) lacking its guanine nucleotide exchange domain (Sakaue et al., 1995), did not block the cAMP‐activation of ERK, showing that SOS does not mediate the cAMP action towards the MAPK cascade. R‐Ras–GRF is another exchange factor for Ras whose activity is enhanced by increased concentrations of intracellular calcium in neurons (Farnsworth et al., 1995; Buchsbaum et al., 1996; Freshney et al., 1997). cAMP, through PKA phosphorylation of specific types of calcium channels, promotes calcium influx into skeletal muscle and hippocampal neurons (Sculptonearu et al., 1993; Hell et al., 1995; Gray et al., 1997). Taken together, these findings suggest that cAMP, through PKA activation, could increase the intracellular concentration of calcium leading to Ras–GRF and Ras activation in these cell systems. In melanocytes, the fact that cAMP‐activation of MAPK is independent of PKA makes the involvement of Ras–GRF in the process very unlikely. Taken together, our data lead us to hypothesize that Ras activation by cAMP in melanocytes could be mediated by an unidentified, cell‐specific Ras exchange factor which would be directly activated by cAMP. Two independent groups have recently cloned several exchange factors for Rap‐1 containing a cAMP‐binding sequence and which are directly activated by cAMP (Epac) (De Rooij et al., 1998) and cAMP‐GEFs (Kawasaki et al., 1998). However, these proteins have not been found to function as exchange factors for Ras. Indeed, we confirmed that Epac was not involved in the cascade leading to ERK activation in B16 cells.
Our data have led us to propose a putative model explaining the cAMP‐activation of the MAPK pathway in melanocytes (Figure 9). We suggest that this process is based on two regulatory and melanocyte‐specific features: (i) a Ras exchange factor directly activated upon cAMP binding, which could account for the cAMP‐induced Ras activation; (ii) expression and activation of B‐Raf kinase, which is required to permit the downstream activation steps towards MAPK since Raf‐1, which is somehow inhibited by cAMP, cannot ensure this function. Future studies will aim to identify melanocyte‐specific Ras exchange factors directly regulated by cAMP.
Materials and methods
Reagents. Forskolin, IBMX, TPA, α‐MSH, insulin, PDGF, 4‐(2‐aminoethyl)benzenesulfonyl fluoride (AEBSF), aprotinin, leupeptin, orthovanadate, NaPPi, NaF, bovine serum albumin (BSA), NGF, gelatin, ATP, protein A–Sepharose and protein G–Sepharose were purchased from Sigma. Dulbecco's modified Eagle medium (DMEM), MCDB medium, Lipofectamine, Optimem, horse serum and streptomycin/penicillin were from Gibco‐BRL. Fetal bovine serum (FBS) was from Hyclone laboratories. [γ‐32P]ATP and the enhanced chemiluminescence (ECL) detection system were from Amersham Life Sciences. Immobilon‐P membranes were from Millipore Corp. MEK–His fusion protein was purchased from Santacruz Biotechnologies. Glutathione–Sepharose beads were from Pharmacia Biotech. The PKA inhibitor H89 was from Calbiochem and the plasmid preparation kit for transfection was from Quiagen. Toxins LT and B were gifts from Dr P.Boquet (U452, INSERM). The FuGene transfection reagent was from Boehringer Mannheim and the Transfast transfection reagent from Promega France.
Antibodies. The polyclonal antibodies against the phosphorylated forms of ERKs and MEK were from Promega France. The specific polyclonal anti‐B‐Raf IS11 antibody directed against amino acids 396–443, which are conserved in both avian and mammalian species, has been previously described (Eychene et al., 1992; Barnier et al., 1995). Polyclonal antibodies against Raf‐1, Rap‐1, ERK2 and SOS were from Santacruz Biotechnology. The antibody to Ras was the monoclonal anti‐pan‐Ras from Calbiochem. The anti‐HA antibody was the monoclonal 12CA5 from Babco (Richmond, CA). The anti‐mouse and anti‐rabbit peroxidase‐conjugated antibodies were purchased from Dakopatts.
Plasmids. The pGEX plasmid encoding the Ral–GDS RBD GST fusion protein is described in Herrmann et al. (1996). The plasmid encoding the B‐Raf RBD GST fusion protein was obtained by subcloning the Ras‐binding domain of B‐Raf (amino acids 146–227 of quail B‐Raf; Papin et al., 1998) into the BamHI and EcoRI sites of pGEX‐2T. The oligomers used for PCR amplification of this fragment were the (+432) 5′‐GTCACGGGGATCCCCTAAGTCTCCACA‐3′ and (670) 5′‐TGGCAGAATTCCCAAGACCTCCAC‐3′. The construct was verified by sequencing. The pcDNA3‐HA‐tagged plasmid containing the ERK1 gene was a gift from Dr Pouyssegur's laboratory (UMR134, Nice), the B‐Raf constitutively active (pcDNA3/HA1‐B‐Raf‐CAAX) was obtained by subcloning the EcoRI–ApaI fragment from pBluescript/B‐Raf‐CAAX (Papin et al., 1998) in place of the EcoRI–ApaI fragment of pcDNA3/HA1‐B‐Raf (Papin et al., 1998). The HA‐tagged constitutively active form of Raf‐1 (pcDNA3/HA1‐Raf‐1‐CAAX) was obtained by subcloning the EcoRV–XbaI 3′ fragment from pRcRSV/HA1‐Raf‐1‐CAAX (Papin et al., 1998) in place of the EcoRV–XbaI 3′ fragment of pcDNA3/HA1 (Papin et al., 1998). The negative mutant of B‐Raf (corresponding to the N‐terminal region of quail B‐Raf) was obtained by subcloning the EcoRI–SalI fragment of pGBT‐9N‐B‐Raf (Papin et al., 1996) into the EcoRI and XhoI sites of pcDNA3. The N‐Raf‐1‐negative form of Raf‐1 (also lacking the C‐terminal kinase domain, amino acids 330–627) is described in Schaap et al. (1993). PcDNA3/HA1‐Ras‐V12 was obtained by subcloning the EcoRI fragment of pGBT‐9/Ras‐V12 (Papin et al., 1996) downstream of the HA1 epitope into the pcDNA3 vector. PcDNA3/HA1‐Ras‐N17 was obtained by subcloning the SalI–XhoI fragment of pRcRSV/Ras‐N17 downstream of the HA1 epitope into the pcDNA3 vector. The plasmid encoding HA‐Rap‐1‐E63 and Rap‐1‐V12 were kindly provided by Dr J.Gunzburg and plasmids encoding Rap‐1‐V12 and Rap‐1‐N17 are described in Vossler et al. (1997) and were tagged with the HA epitope. The plasmid encoding the SOS mutant ΔSOS was obtained from Sakaue et al. (1995). The vector encoding the EpacΔcAMP construct was from De Rooij et al. (1998).
Cell culture and specific cell treatments
B16/F10 mouse melanoma cells and NIH 3T3 mouse fibroblasts were cultured in DMEM supplemented with 7% FBS and penicillin/streptomycin [100 IU (50 μg)/ml] in a humidified atmosphere containing 5% CO2 in air at 37°C. Normal human melanocytes were obtained from neonatal foreskins of Caucasian individuals, and grown in MCDB medium according to a modification of the method of Eisinger and Marko (1982) as described previously (Aberdam et al., 1993). Before kinase assays or pull‐down experiments, cells were depleted of growth factors for at least 24 h.
When indicated, cells were treated with forskolin (20 μM), IBMX (100 μM), TPA (16 nM), α‐MSH (1 μM), PDGF (5 ng/ml) or insulin (0.1 μM) for the times indicated. Cells were incubated with C.sordelii LT at 70 ng/ml for ≥4 h before other treatment or with C.difficile toxin B at 0.5 g/ml for ≥4 h before any treatment. To inhibit PKA activity, cells were treated with H89 at 3 μM for 20 min and then with cAMP‐elevating agents for another 10 min.
CHO‐IR cells stably expressing the insulin receptor were obtained from Dr Tartare‐Deckert (INSERM Unité 145, Nice, France) and cultured in F12 medium supplemented with 10% FBS. PC12 cells from the American Type Culture Collection (CRL‐1721), from Dr Schlessinger's laboratory (Dikic et al., 1994) and from Dr Rogers' laboratory (Walton et al., 1988) were cultured in DMEM supplemented with 7% horse serum, 7% FBS and 1 mM glutamine. Before transfection, PC12 cells were seeded on dishes coated with collagen.
Western blotting
Cells were grown in six‐well dishes, starved of serum for 24 h, treated with agents as indicated and lysed in a buffer containing 1% Triton X‐100, 50 mM Tris pH 7.6, 100 mM NaCl, 50 mM NaF, 5 mM EDTA, 1 mM NaPPi, 5 μg/ml leupeptin, 1 mM AEBSF, 100 IU/ml aprotinin, 1 mM NaVO4 and 10 mM p‐nitrophenolphosphate. Proteins (30 μg) were separated on 10% sodium dodecylsulfate (SDS)–polyacrylamide gels and transferred to Immobilon‐P membranes. Membranes were saturated and proteins were detected with the appropiate primary antibody and a secondary peroxidase‐conjugated anti‐mouse or anti‐rabbit antibody at a dilution of one in 3000. Blots were developed using the enhanced ECL system.
B‐Raf and Raf‐1 immunokinase assays
B16 cells were grown in 100 mm dishes. After the indicated stimulations, cells were washed and lysed. For B‐Raf immunoprecipitation, cells were solubilized in buffer containing 50 mM HEPES pH 7.50, 50 mM NaCl, 50 mM NaF, 10 mM NaPPi, 100 μM sodium orthovanadate, 100 μM AEBSF, 100 IU/ml aprotinin, 1 mg/ml leupeptin and 1% Triton X‐100. Extracts were incubated with 2.5 μl of the anti‐B‐Raf polyclonal antibody (IS11) and the kinase assay was performed as described by Barnier et al. (1995). For Raf‐1 kinase assays, cells were lysed in buffer containing 50 mM HEPES pH 7.4, 150 mM NaCl, 10 mM EDTA, 100 mM NaF, 10 mM NaPPi, 2 μM sodium orthovanadate, 100 μM AEBSF, 5 μg/ml leupeptin and 1% Triton X‐100. Solubilized proteins were incubated with 10 μl of the anti‐Raf‐1 polyclonal antibody pre‐adsorbed to protein A–Sepharose and the kinase assay was performed as previously described (Englaro et al., 1995) using purified His–MEK‐1 as a substrate. Reactions were stopped by addition of Laemmli buffer and analysed by SDS–PAGE (10% acrylamide) and autoradiography.
Cotransfection and HA‐immunoprecipitation assays
Since the efficiency of transfection in B16 cells appears to be very low, we tested the action of different effector proteins on ERK activation in these cells as follows. B16 melanoma cells were seeded in six‐well dishes and transient transfections were performed the following day using 9.8 μl of Lipofectamine and 3 μg of total plasmid DNA (1.5 μg of pCDNA3 HA–ERK1 and 1.5 μg of plasmids encoding the various mutant cDNAs) in 1 ml final volume of Optimem. Cells were then starved of serum, treated with agents as indicated and lysed in a 1% Triton buffer as described previously. Equal amounts of protein extracts were incubated with 15 μl of the anti‐HA monoclonal antibody and protein G–Sepharose was used to collect the antigen–antibody complexes. Immunoprecipitates were washed in 0.1% Triton buffer containing 30 mM HEPES pH 7.4 and 30 mM NaCl, and resolved on 10% SDS–polyacrylamide gels. Gels were transferred to Immobilon‐P membranes, probed with a polyclonal antibody against active ERKs and visualized by ECL. Proteins (30 μg) were probed with an anti‐tag antibody to detect exogenous ERK1 expression. We used the FuGene reagent (Boehringer Mannheim) to transfect CHO cells, and the Transfast reagent (Promega) to transfect PC12 cells, as described in the manufacturers' protocols.
Pull‐down experiments to detect activated Ras and Rap‐1
B16 mouse melanoma cells, NIH 3T3 cells or PC12 cells were grown to 80% confluence and stimulated with agents. Cells were then washed twice with ice‐cold phosphate‐buffered saline (PBS) and lysed in buffer A containing 50 mM Tris pH 7.5, 15 mM NaCl, 20 mM MgCl2, 5 mM EGTA, 1% Triton X‐100, 1% N‐octylglucoside, 100 μM AEBSF, 5 μg/ml leupeptin and 1 mM pepstatin A. Lysates were clarified by centrifugation and supernatants were incubated with 30 μg of GST fusion protein precoupled to glutathione–Sepharose beads. To isolate Rap‐1–GTP, we used the GST–Ral GDS RBD obtained as described by Herrmann et al. (1996). To detect Ras–GTP, the GST–B‐Raf RBD, obtained as described by Herrmann et al. (1995), was used. After incubation for 2 h at 4°C, beads were washed three times in buffer A, resuspended in Laemmli buffer and boiled. Samples were analysed by SDS–PAGE (12.5%) followed by transfer to Immobilon‐P membranes. Active Rap‐1 and Ras were detected using specific antibodies, as described above.
PKA activity assay
B16 cells were grown in 100 mm dishes, then stimulated as described and lysed in a buffer containing 50 mM HEPES pH 7.6, 150 mM NaCl, 10 mM EDTA, 10 mM NaPPi, 2 mM sodium orthovanadate, 100 mM NaF, 0.5 mM AEBSF, 100 UI/ml aprotinin, 5 μg/ml leupeptin and 1% Triton X‐100. The lysates were incubated with phosphorylation buffer containing 10 mM HEPES pH 7.2, 68.5 mM NaCl, 2.7 mM KCl, 0.15 mM KH2PO4, 0.5 mg/ml glucose, 25 mM β‐glycerophosphate pH 7.2, 10 mM MgCl2, 1 mM EGTA, 1.85 mM CaCl2, 0.1 mM ATP, 100 μM Kemptide as a substrate peptide and 25 μCi of [γ‐32P]ATP per mmol. The phosphorylation reaction was allowed to proceed for 10 min at 37°C and then stopped by spotting on to Whatman P81 papers. The papers were washed twice with 1% (v/v) orthophosphoric acid, rinsed in ethanol and air dried. The radioactivity was determined by Cerenkov counting.
We thank Dr de Gunzburg for providing vectors encoding Rap‐1‐N17, Rap‐1‐V12 and Rap‐1‐E63, and Dr P.Stork for providing other Rap‐1‐N17‐ and Rap‐1‐V12‐encoding plasmids. We thank Dr Schapp for the dominant‐negative version of Raf‐1 (N‐Raf‐1), Dr Pouyssegur for HA‐tagged ERK1, Dr Tartare‐Deckert for the CHO‐IR cells and Dr Bos for the EpacΔcAMP construct. We are grateful to Dr Boquet for the C.sordelii LT toxin and the C.difficile B toxin, and Aurore Grima and Christine Ordonez for scanning the autoradiography films. We are grateful to Dr Boulukos and Dr Pouyssegur for critical reading of this manuscript and to Alexandra Charlesworth for her expert editorial help. This work was supported by the Association pour la Recherche sur le Cancer (ARC‐grant 5209), La Ligue contre le Cancer and the Centre de Recherche et d'Investigations Epidermiques et Sensorielles (CERIES).
- Copyright © 2000 European Molecular Biology Organization


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We hope you can join us on August 18, 2018 for God's Girls!
How do you view yourself? Do you view yourself like God sees you or do you view yourself as though you are looking in a distorted mirror? Our world is constantly nagging at us to see ourselves and others in a distorted way. Let's look at how God views us and how we should view others.
Girls in grades 6th – 12th, please join us for this fantastic event! You can find more information below.
Our Keynote Speaker: Charissa Miller
Charissa Miller resides in Highland Village, Texas with her husband, Michael, where she attends and serves as a member of the Lewisville church of Christ. Charissa has been active in the Lord's church for her entire life, and she has a strong passion for mission work and for teaching young children, teenaged girls, and women. Her passion for teaching teenaged girls and women has allowed her to teach girls' Bible study groups, to speak at girls' and ladies' events and conferences, and to serve as a counselor and mentor at church camps and youth retreats. She has been speaking professionally since 2011 and feels honored, humbled, and excited for this opportunity.
Our Breakout Speakers:
Tiffany Frye Sarah Dirrim Kellie Hudson
Jessica Ashley Carli Etheridge


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Beer Line Cleaning 2-GO
Line Cleaning 2-GO
Line Cleaning 2-GO system has a 5 quart hand pump reservoir with a 25" line with a sanke duplex cleaning coupler attached at the line. It also includes a faucet brush, faucet wrench, and 4 oz bottle of line cleaner (mix 1/2 oz per quart of water). Simply disengage the sanke, remove the beer line from the sanke, connect the beer line to the cleaning coupler and pump solution (or clean water) back through your line and out the faucet. The 5 quart solution capacity is good for even large set-ups!
There are 2 additional options you can select from below.
Option #1:
If you want to use this pump on both commercial and corny kegs, you will need to add the 1/4'' MFL tailpiece assembly. As long as you use 1/4'' MFL beer disconnects on your corny kegs, this option will work with this pump.
Option #2
We have a new fitting for ball locks that will allow you to clean your lines with out removing the fittings from the lines. It can't get any easier than that! You will need to add this option for the ball lock fitting.
You do not need both options to clean your lines, this option is for convenience of not having to remove your line from the fitting and you will not need option #1 as you will get everything you need with option #2 to clean your lines.
(This fitting will only work with ball lock disconnects)
If pump does not pressurize tank, use a food grade grease on the outside of the plunger o-ring
Adventures in Homebrewing
Purchase / Buy


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The boat we bought
In 2015, Teal was 12 years old with less than 300 hours (approx) on the engines – 25 hours per year!
The boat was beautifully maintained, but we had to be concerned about the low level of use.
We had a special problem. Dairne had had a stroke, and was not very mobile.
We had to devise ways of getting on board easily, and coping with the rather high steps from the deck into the cabin, and from the saloon, into the galley (forward) and the owners cabin (aft).
See the 'mobility access' tab on the menu to the right
Key Issues
The previous owners had kept Teal in a marina, plugged into shore power. That was not our way of sailing.
We like to spend days away in anchorages like Newtown and Keyhaven.
We keep our boat on a swinging mooring at Marchwood. It is easier to pick uo a mooring short handed rather than backing into a marina berth. BUT you need a tender to get ashore.
Our solution was to install a 4kw Fischer Panda generator (the space for which had been designed into the boat), and to add snap davits so we could go on using the 8ft Walker Bay dinghy that we already owned.
Overall Dimensions
Length (Hull): 10.7m (35'1″)
Beam: 3.8m (12'6″)
Draft: 1.1m (3'7″)
Airdraft (Mast down): 3.44m (11'3″)
Displacement: 9,000kg
Built 2003
GRP Hull, deck and superstructure
Teak laid decks
2 x Perkins Sabre 265Ti 265hp diesel engines
6 cylinder 6 litre motors with turbochargers and intercooling
Fresh water cooling
Maximum speed 17 knots approx
Cruising speed 15 knots
500 hours run (approx) at April 2019
Vetus single lever electronic throttles/shifts (duplicated on flybridge)
Shaft drive to four blade bronze propellers
Eltrim trim tab controls (duplicated on flybridge)
Cutlass bearings and deep sea seals replaced in 2012
Eltrim trim tabs with indicators
Vetus bow thruster
4 x AGM Batteries (New 2011) with isolators
Charged by engine alternator and 240v shore power battery charger
Fischer Panda 4kw generator installed 2015 (150 hrs at end 2018)
240v Shore power ring main
12v accessory outlets
24v solar panels switchable between battery banks installed 2019
2 x 608 litre (134 gallon) stainless steel fuel tanks
1 x 350 litre (77 gallon) stainless steel water tank
Pressurised hot and cold water system
Water heated by engine calorifier and 240v shore power immersion heater
Also heated via Eberspacher cabin heating system
Sleeps six in three double berths in two cabins and the saloon
Eberspacher diesel fired warm air heating with outlets to all cabins (also heats water)
Double V Berth with storage below
LED reading lights over bunks (2019)
High level storage lockers
Hanging locker
Overhead hatch to deck with retractable blind
2 x Opening port hatches
Electric sea toilet, fresh water flush (2018)
Porcelain hand basin with hot and cold mixer/shower wand
Storage lockers
Shower curtain
Stainless steel double sink with hot and cold mixer
Plastimo Neptune 2000 two burner gas cooker with grill and oven
Waeco refrigerator. With freezer compartment
High and low level storage lockers
Opening port hatch
C shaped converts to a double berth
Height adjustable saloon table
Engel refrigerator
Fold down coffee table with 12v accessory outlet below
2 x Moveable seats/lockers
KAB 525 helm seat with suspension
Folding double passenger seat
Large chart. table with chart storage
Overhead electrical distribution panel
Full width aft cabin
Double berth. LED reading lights over (2019)
Numerous storage lockers and hanging locker
Dressing table with mirror
Overhead hatch to deck with retractable blind
2 x Opening port hatches
Jabsco sea toilet
Porcelain handbasin with hot and cold mixer/shower wand
Storage lockers
Towel rail and mirror
Shower curtain
Raymarine C90W chartplotter/radar display (New 2013)
Raymarine 230 DSC VHF remote speaker
(Portable ICOM VHF replaces failed VHF handset)
Raymarine ST6001 Autopilot
Raymarine ST60 Tridata (Log, speed and depth)
Raymarine C120W chartplotter/radar display (New 2013)
Raymarine 230 DSC VHF Handset with remote speaker
Raymarine ST6001+ Autopilot
Raymarine ST60 Tridata (Log, speed and depth)
Raymarine Raydome (New 2013)
Raymarine AIS (installed 2015)
Raymarine GPS (replaced 2017)
Raymarine Smart wireless remote controller
Raymarine rear view camera (installed 2015)
Navigation lights
Horn (replaced 2017)
Firdell radar reflector on mast (2019)
Teak table for the aft deck
Bimini cover for aft deck
Pushpit mounted outboard bracket
Teak bathing platform
Boarding ladder to bathing platform
Hot and cold transom shower
Exterior seat cushions
Electric (automatic) and manual bilge pumps
Windscreen washers, wipers and demister
Plastimo clock and barometer
Stereo radio/CD player
Portable TV/video player (added 2016)
Special boarding ladder for disabled crew(added 2015)
Extra internal steps for disabled crew (added 2016)
8ft Walker Bay tender on Snap Davits (installed 2016)
Minn Kota electric outboard (Installed Sep 2017)
The need
The modifications described here have proved beneficial to all who have used them. In particular, as we get older, climbing on and off boats, and mounting ladders gets increasingly difficult. In our case, I was 75 and Dairne was 74 in 2016. Also, she had quite a severe left side stroke in 2012. She walks with a stick, very slowly, and uses a wheelchair for any significant distance (roughly more than 50 metres).
Getting on board
Many motorboats rely on access via the swimming platform at the stern. Few have handholds that meet the needs of anyone with mobility impairment. Teal is far better in this respect having midship access, but it is a couple of feet above the pontoon. We had a purpose designed 3 step boarding ladder made which was as wide as possible, another feature required by those with impaired mobility. It turned out to be quite a challenge to my friends who made it, but the result is excellent. The ladder stows under the saloon seats when not in use.
The other essential was a hand grab mounted on the saloon side. We had to be careful as the securing screws go through into a cable duct!
Internal Access
Some motorboats have a better walkthrough thanTeal, but all we have seen rely on boarding via the swimming platform. So we had to overcome the level difference between the side deck and the main saloon sole. As built there are is one step between these levels. We added an additional portable step on each side, secured with quick release clips or wingnuts so access to hatches and lockers below was not compromised.
The steps down into the cabin aft and the galley forward are steep, and the rise of each step is much more than the standard maximum step rise of 7 inches. Our solution was to add portable half steps secured by quick release clips to allow access to lockers below the steps.
These work well, but we have yet to provide proper handholds on both sides as required by a stroke survivor.
Dairne uses a standard NHS wheelchair which folds up. It stows in a specially made zipped water resistant bag that lashes to the guardrails across the transom. Access is only slightly impaired,
Cruising needs
Teal had always been kept in a marina, almost permanently plugged in to shore power.
With less than 300 hours on the engines in 12 years, she had not had much use. We, on the other hand, would want to visit places like Newtown, Keyhaven, Chichester, and South Deep in Poole harbour. In all these harbours we would be at anchor, and would not have access to shore power. And Teal has 2 fridges to sustain!
Although we kept Teal in the new Yacht Haven at Royal Southern YC in Hamble for the first winter, our intention was to keep her in the summer on a swinging mooring at Marchwood. Once again, we would not have access to shore power.
Luckily, the Hardy Commodore 36 was designed to have a generator, and we found that the space had not been compromised. Even more fortunate was that the supplier, Fischer Panda, were located nearby at Ringwood. So the generator was installed in Poole where the boat was bought before we made the delivery trip to Marchwood in Southampton Water.
The Tender
On a mooring we would also need a tender. Teal had no dinghy (other than the liferaft).
We already had an 8ft Walker Bay dinghy which, with its inflatable fender would make an excellent tender. But its curved sides would not work on standard snap davits on the swimming platform. Eventually we found that Weaver, the Snap Davit manufacturer had developed a frame to take the Walker Bay. We think we were the first to import the kit from the USA. It was expensive, but it works.
The only downside is that it adds quite a lot of weight to the dinghy.
It also means that we have a sailing dinghy to use when visiting the serene harbours mentioned earlier.
Solar Panels to charge either battery bank
LED reading lights in aft cabin and fcle
Firdell radar reflector
Solar charge connection for G-tech floor cleaner
New mixer tap in aft cabin
LED riding light
Installed deckwash pump
Installed electric toilet in aft cabin
Replaced throttle system. (Failed at end of 2016. Advised by Vetus that it was obsolete)
Installed snap davits for Walker Bay (see Essential Mods)
End 2015
Added steps and boarding ladder (see Mobility Access)
Replaced anchor with 20kg Bruce; CQR to locker on deck (Bruce would not fit)
Transferred hotplate and electric kettle from Ariadne
Replaced gas alarm with gas/CO alarm; convert to propane
Added 2 bookcases
Installed Wireless autopilot remote control (ex Ariadne)
.Installed AIS (and aerial splitter)
Installed Rear View camera
Installed Fischer Panda 4kw generator
On this page, the omissions from the current specification that are desirable are noted
LED lights
Th anchor light has been replaced with LED. I cannot find bulbs to fit the saloon light fittings, so the entire fittings need replacing. Advice being sought from Hardy.
The Navtex was removed from Ariadne. But so much weather data is now available by intern et and mobile phone that it is questionable whether it is worth installing on Teal.
We carry a small portable 12v TV which we use occasionally. A permanent location for the aerial would be desirable.
Alarm System
There is an alarm system that connects to a mobile phone that we never got round to installing on Ariadne. I really must get round to putting it on Teal!


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NBC's new musical series, Rise—think Friday Night Lights meet Glee—is already making headlines even before the first episode premieres because it was revealed at the Television Critics Association panel that the show's main character is not gay like he is in the book the show is based on.
Rise is inspired by the book, Drama High, based on the true story of Lou Volpe, a teacher who mounted a production of Spring Awakening at his high school in a small, blue-collar town.
In real life Volpe was closeted, and came out as gay later in life—but in Rise the character based on him, Lou Mazzuchelli (Josh Radnor), won't come out because he won't be closeted. Series executive producer Jason Katims decided to make Lou a straight family man.
"We took [the book] as an inspiration, and then I really felt like I needed to make it my own story," Katims said this week at the TCA panel. "With Lou's family life and Lou's family itself, there's a lot of reimagination. Not just in terms of gay or straight, but in terms of the family structure."
Critics were quick with their responses once they learned of the sexuality change to the show's lead character.
"A story about a closeted gay man putting on Spring Awakening sounds a lot more interesting than a story about another Mr. Schue," tweeted The Daily Beast's Ira Madison III, referring to the straight theater teacher from Glee.
A story about a closeted gay man putting on Spring Awakening sounds a lot more interesting than a story about another Mr. Schue https://t.co/SMKGM5AWmK
— Ira Madison III (@ira) January 10, 2018
Katims, who is known as the man behind Friday Night Lights and Parenthood, promised that sexuality and LGBT issues would be dealt with on Rise—which would be hard to avoid since the musical the school is mounting, Spring Awakening, is all about teenagers discovering their sexuality and features a gay storyline.
"I was inspired to tell the story of Michael (Ellie Desautels), this transgender character, and Simon (Ted Sutherland) who's dealing with his sexuality and growing up in a very conservative religious family," explained Katims.
"Those stories felt like they resonated with me as a storyteller, I wanted to lean into that."
Making the character based on Volpe straight is disappointing, but Hollywood has a history of changing queer characters from books straight when the stories are adapted for the screen.
Paul Varjak was gay in Truman Capote's Breakfast at Tiffany's novella, but then turned straight when George Peppard played him in the film version, and the lesbian elements from The Color Purple were largely removed when Steven Spielberg brought the book to the big screen—just two of many examples.
Without the closeted teacher will you watch Rise when it premieres March 20 on NBC?


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NM Form 76 Easement - Damage or Enforced Removal Endorsement (ALTA Form 28-06, 10-16-08)
Easement - Damage or Enforced Removal Endorsement
Attached to Policy No.____
Issued By
The Company insures against loss or damage sustained by the Insured by reason of:
(1) damage to an existing building located on the Land, or
(2) enforced removal or alteration of an existing building located on the Land, as a result of the exercise of the right of use or maintenance of the easement referred to in Exception _____ of Schedule B for the purpose for which it was granted or reserved.
This endorsement is issued as part of the policy. Except as it expressly states, it does not (i) modify any of the terms and provisions of the policy, (ii) modify any prior endorsements, (iii) extend the Date of Policy, or (iv) increase the Amount of Insurance. To the extent a provision of the policy or a previous endorsement is inconsistent with an express provision of this endorsement, this endorsement controls. Otherwise, this endorsement is subject to all of the terms and provisions of the policy and of any prior endorsements.
[Witness clause optional]
Authorized signatory_____________
For issuing guidelines on this form, see Guidelines


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NW6.5 sp7
GW 8 hp1
I upgraded to GW8 about a month ago. Everything has gone without a hitch. I
had a mail relay in place that GW relayed all outbound email to. Again,
there have been no issues with this set up.
Recently, the relay was removed, MX record changed from the mail relay to
the GW server. I made sure that there was a reverse DNS lookup for the new
MX record with our ISP.
Now, out of the all of the emails that are sent each day, I have a handful
of them that keep failing with a 501 5.5.4 Invalid address on the server. I
am also getting a couple of 501 Invalid Domain Name errors on the server
also. They are always to the same domain. My mail server points to my
internal dns server that forwards all external requests to my ISP's dns
Any idea what I can do to fix the problem?


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Great Northern States Health Care Initiative
The supple leather-based cover bends beneath your fingertips as you open to the first web page; you inscribe your identify in your own authentic scrawl. Then we squeeze all our beingness into the frames of those labels which identify us, limit us, and dupe us out of our aware wanting. It by no means crosses our minds that society is made up of people, and if every individual individually and privately selected constructive and constructive ways of being, there could be no political or social issues to which to commit our efforts.
I assumed it might cowl things," Mr. Scott stated. But as soon as he needed it, he realized the plan limited what it paid for outpatient care to $2,000 a 12 months, and all of his treatment, from chemotherapy to CT scans, seemed to fall in that class. Good day Lee Cloak, thank you a lot for reading and sharing your expertise. I'm so sorry for not responding earlier. I used to be away for a very long time.
Through the fall and spring semesters, you'll be able to discuss with an authorized health professional after hours by calling (855) 303-2631. The examine additionally suggested that in their pre-college years, minority youngsters eat extra fast food, drink extra sugar-sweetened drinks, and usually tend to have TVs of their rooms, compared to Caucasian youngsters. Strain the liquid and mix with honey and lemon juice to taste. Take two tablespoons of this pure syrup thrice a day and you may see a immediate reduction of dry cough.
Anytime you fly, it is important to be aware of your surroundings. Don't watch baggage for a stranger or pick up one thing that is not yours. And keep all of your items with you and accounted for. There are 7 steps to … Read More ...


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This page uses TLS encryption to keep your data secure.
High Holidays 2018
In this Section
Ongoing Schedule
Schedule for every Shabbat (Sat) Morning
- 9:15-10 AM Cake and Kabbalah class (no prior knowledge necessary. All welcome)
- 10 AM-10:45 AM - Hebrew service
- 10:45- 12:15 PM Torah reading, discussion and main service
- 12:15 PM Kiddush
Upcoming Events


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Added: 2018-06-15
Category: blocked drains
Comments: 0
To be able to take advantage of the incentive payment must be made by bank transfer. Boilers are an energy efficient and environmentally friendly mode of heating they work by cycling cold water through a series of heated pipes before distributing it throughout your home as either hot water or steam. Formed way back in 1866, baxi produce a selection of high efficiency boilers, such as baxi platinum combi he, baxi duo-tec combi he, baxi solo he and.


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Gust and its variants have been characterized by its strong armour and mobility, but rather mediocre output. These suggests that it would make good assault wanzers. Its two arms can be internally equipped with machineguns. However, in later appearance, it is seen with standard arms. If these are variants of the same model or not is not explicitly stated. Gust seems to have proven itself to be competent assault units, and is widely deployed by the U.S.N. Army, as they were seen being piloted by U.S.N. assaults in Huffman Island. Gust and its variants were also seen being deployed by U.S.N. army when it attempt to regain control of Venezuela and when it invaded the Madeira Island. However, they were not exclusive to the U.S.N. since the Revolutionary Army in Alordesh were also seen employing Gust wanzers.
The Gust wanzer model has two branches series, namely the Vapor and the Storm.
- U.S.N. Huffman, primarily as assaults (Front Mission First, Online, 5)
- Alordesh State Army, primarily as assaults (Front Mission 2)
- E.C. Britain, primarily as assaults (Front Mission 4)
- E.C. Poland, primarily as assaults (Front Mission 4)
- U.S.N. Venezuela, primarily as assaults (Front Mission 4)
- Gust (Front Mission First, 5, Online)
- Gust 500 (Front Mission 4)
- Gust 503 (Front Mission 4)
- Gust 503A (Front Mission 4)
- Gust 503B (Front Mission 2)
- Gust 505A (Front Mission 2)
- Gust 505C (Front Mission 2) - the final variant of Gust series, as Diable ceased its production in 2097.
- Vapor (Front Mission 5)Both
- Vapor 2 (Front Mission 5)
- Storm (Front Mission 5)
Known PilotsEdit
- Luis Perez (Storm), Front Mission 5
- Ines Torres (Storm), Front Mission 5
- Carl Thammond (Gust), Front Mission 5
Trivia Edit
- There is a wanzer model named Vapor Sand, although it is not known to be related to the Gust series.
- By 2102 (Front Mission 2), approximately there are 250 Gusts in active military service worldwide.


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We've been in the car for nine days now, driving across all of Brazil and Bolivia (with two hotel rooms throughout. lots of car sleeping). We're finally in Ororu, Bolivia, heading south to the Salar de Uyuni (world's largest salt desert) today. So far, we like Bolivia (except for the police, who are corrupt and awful). It's cheap, the wine is finally decent again after disgusting alcoholic grape juice in Brazil, and we had the best pizza of the trip in Santa Cruz, Bolivia - so good, I almost wanted to stay another night to eat there again for lunch the next day.
One very strange thing about Bolivia - the gas here is extremely cheap, but if you want the cheap, subsidized gas, you have to sort of steal it. I don't feel too bad about this after dealing with the corrupt police here. So, if we pull into a gas station with our foreign-plated car, they won't charge us the regular rate for gas - they'll charge almost three times more. But some places, if I get out our gas can and point to it, they'll fill the car for the cheap rate. Or sometimes they'll fill the gas can directly (which is a pain, because it takes two of these to fill the car's gas tank). Or sometimes they'll refuse us altogether, at which point we'll drive away, park off the lot, and walk back to the gas station with the empty gas can. So far we haven't had to pay the premium price for gas throughout Bolivia, but it's a giant pain to lug a 20-liter can up the road every time we have to get gas - which is often, when you're driving about 18 hours a day.
After sleeping in the car on another icy night in the altoplano (high plains), we visited a hot springs the next morning to thaw our feet. We'd also climbed from 200m above sea level straight up to about 3,600m the previous day, and about five minutes after I climbed into one of the hotter baths at the hot springs, I got violently ill. I'm not sure if it was from the drastic temperature change or altitude change or both, but after throwing up the past day's diet of water, I was basically fine again, though still a little winded here in Oruro. Anyway, here's the first half of Bolivia (the more stunning half starts today, hopefully):
|We miss first world roads so much.
|Occupy Bolivia?
|One of many, many, many streetside fires we've seen. Western Brazil and eastern Bolivia's roadsides are seemingly perpetually on fire.
|View from our hotel room in Oruro. We splurged and spent about $28 for a massive suite.


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Grey Skies Are Gonna Clear Up
I don't do this often, post about non-book related things on here, but I simply cannot help it! I'M SO EXCITED. AND I JUST CAN'T HIDE IT.
In the real world, I'm a nurse aide at a senior living community. I love my job - but I hate hate hate the people I work for. I got a job offer today at substantially more than I make now doing what I do now, but with the proper resources and support from management! And these people don't put how much the residents pay first, they actually put THEM first!!!!!!!! AND I'm going to actually get a lunch break for the first time in a goddamn year!


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It's Time to Roller Skate
Join us skating at San Diego's only wood roller skating rink. Groove to all your favorite songs from back in the day and today!
Celebrate and skate!
Follow Us!
We love skating.
We love our history.
Skateworld is celebrating its 44th anniversary in October and continues to offer the highest quality customer service for all your family entertainment needs. Our biggest goal, even today, is to help promote an active lifestyle while embracing the need for family or social activities.
With its building billed as a historic resource, HRB #948, Skateworld is dedicated to preserving the look and feel of a building dedicated by Eleanor Roosevelt when it opened in 1941 as the Tenant Activity Building, most notably the many arches that span the entire width of the skating floor and go 9 feet into the ground on either side.


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Tagged: Phillies
Prediction for Postseason
I know that it's been too long since my last post, but there are actually more important things in life than the Dodgers (gasp). Anyway, while there was a bit of fear there, our boys did win the division and finished with the best record in the National League.
That being said, here are my predictions for the postseason. I think that, at the most, there will be one upset with the Twins possibly taking out the Yankees. The Dodgers will beat St. Louis, Phillies over Rockies (they've already won the first game) and the Angels will take down Boston.
I'll go out on a limb here and say that the Dodgers will play the winner of the Yankees / Twins series in the World Series.
Update: Technically the Rockies aren't the underdog since they finished with a better record than the Phils, but because they're the wild card, I'm calling them the underdog here.
Unruly Fans and Baseball
The Dodgers had yesterday off, but I wanted to take a moment and write a quick post about what happened to Shane Victorino of the Phillies during a game at Wrigley Field. For those of you who haven't heard, a Cubs fan threw a beer, cup and all, at Victorino as he was catching a long fly by Jake Fox.
The fan initially escaped as security grabbed the wrong guy, but has since turned himself in. Victorino filed a complaint with the police before the 21-year-old perpetrator finally did the right thing. I'm not using his name because the guy doesn't deserve any fame for his stupidity.
The Cubs apologized to Victorino on behalf of the entire organization and fans, and Victorino has been really gracious about the whole thing.
These incidents are rare, but they do happen. If the Cubs didn't sell beer the guy probably would've thrown a soft-drink or something else. Security was on the area (but the wrong guy) quickly. There really isn't anything else that the Cubs organization could've done to prevent this from happening.
These rare incidents also aren't new. Somebody threw a whole chair at Roger Maris when he was in the home run race with Micky Mantle. He thankfully missed.
Whether these losers are throwing cups or furniture or syringes (at Barry Bonds) at players or yelling obscenities at rival fans, they ruin the game for everyone. Grow up people. It's a game.


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I made this pizza tonight. It is inspired by Bev, one of my favorite food bloggers. Grilled chicken, grilled orange and yellow peppers, grilled red onion, sweet local corn, and a tomato fresh from my garden all piled on top of a crispy crust slathered in pesto from last years garden, coated with stringy mozzarella cheese, drizzled with olive oil, and sprinkled with freshly picked basil and parsley.
If summer was a pizza, this would be it. It was a celebration of summer, and gardens, and rain, because we've had a lot more of that this year and that's made my garden oh so happy.
It was a celebration for Bev, who I have never met, but am totally smitten with because of what she cooks and how she writes and her two parasites. She's expecting twins. Its not a secret. I'm thrilled for her. And she's using her blog to educate the interwebs about IVF. She's dispelling myths. She's a rockstar like that. I think we are kindred sisters. I'm probably blocked from commenting on her blog now forever because this is starting to sound a leetle bit stalkerish. Sorry Bev! I love ya! In a non threatening way!
We scarfed this pizza while watching the first football game of the season. I am ready for fall and football but not for the whole town to be overrun by college students. That's the funny thing about college towns. There are college students. Lots of them. Annoyingly unavoidable.
I digress.
This pizza was a celebration of football. And watching football in the blissful relaxation that is sitting on the couch and not getting up to go help a certain small person fall asleep because he rocks at that now. Best baby ever. EVER.
This pizza was a celebration of motherhood.
Maybe you had to be there.
What does the end of summer taste like to you?


text: On the main column (main-column.php) on the home page, the post doesn't honor paragraph breaks, which makes it look like one big paragraph. I'm a professional author (published five books) and it's important that I have these paragraph breaks. Also, is there a way to add a photo from that same blog post to show with the text and honoring the alignment from the original post? Please keep in mind, I'm no coder, but this is looking really great if I can get those para breaks. Thanks, rg.


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Today is time for Keep & Share. It is an unusual recommendation, considering that I am a knitter (alas capable of knitting things up myself), but I still think it is well worth knowing.
Here is why (besides that it is a lovely idea):
- all things are knitted up by skillful clever people in UK (not everything is made in China after all)
- is far more sounder in terms of sustainable thinking than acquiring a load of fashion fads, which will be so out of date three months later that it is simply not true (just think what we could do with all energy we put into being slaves of fashion and invest in long haul pieces instead)
- provides service that is tailored to suit individual needs
- is unique and taking care of a dreadful gap in the marketplace
- it is a real tribute to a more original and personal attitude towards dressing
For all those reasons and possibly quite few others, which I won't go into right now as I am running desperately short of time this morning, you would be smart to remember it. You never know! To give you an example, last year I had a baby and was so busy getting used to a new little person in the family that I had absolutely no time to knit or even think about knitting. So I got one of those lovely cardis as a treat for myself for getting along so well, and also because it was getting colder and colder as I was being faced with the eternal "I've got nothing to wear" (which actually, as I think about it, was perfectly normal given that pregnancy had left me completely unable to squeeze into any of my favourite clothes). I love that cardi to bits, and it felt good knowing that my indulgence was helping another knitter to thrive!
Well done Amy. And all the very best!


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Position: Co-Chief Executive Officer, Alternate Governor, Boston Bruins
Jeremy M. Jacobs Jr. is Co-Chief Executive Officer of Delaware North, a family-owned, global leader in hospitality and food service. Delaware North has annual revenue of $3 billion and more than 55,000 employees, and it serves half a billion customers annually on four continents.
As Co-CEO, Jacobs provides stewardship to the more than 100-year-old Delaware North and its operating subsidiaries, which include industry leaders in food and retail operations at airports and sports venues, sports facility ownership and management, operations of parks and major tourist attractions, hotel ownership and management, and gaming operations. The company recently acquired Patina Restaurant Group, a leader in the premium segment of the restaurant and catering industry that operates restaurants and manages catering and food service at high-profile venues such as Rockefeller Center in New York, the Emmy Awards Governors Ball in Los Angeles, and Walt Disney World in Florida and Disneyland in California.
In his position, Jacobs is responsible for long-term strategic direction, determining mergers and acquisition candidates, positioning the company in emerging markets, and working with financial institutions on overall business strategy. In addition to his senior management post with Delaware North, Jacobs serves as alternate governor for the six-time Stanley Cup winning Boston Bruins of the National Hockey League.
Jacobs's professional involvement with Delaware North began more than 30 years ago. He was named chairman of Delaware North's flagship subsidiary, Sportservice, in 1995 and successfully developed and launched name-brand initiatives in retail and fine dining. Under his leadership, Sportservice flourished and today includes contracts with some of the world's most high-profile sports clients and venues, including the St. Louis Cardinals at Busch Stadium, the Green Bay Packers at Lambeau Field, and the New York Jets and Giants at MetLife Stadium, as well as London's Wembley Stadium and the Sydney Cricket Ground.
Jacobs was named executive vice president of Delaware North in 1991. Prior to joining the company he was a financial analyst with the Money Market Group at Paine-Webber, Inc. in New York. He has a Masters of Business Administration from the Wharton School of Business at the University of Pennsylvania and a Bachelor of Arts degree from Georgetown University. Jerry met his wife, Alice Jacobs, when they were both students at the University of Pennsylvania, where she earned a Juris Doctor degree. Alice is the chair emerita of the Western New York Women's Foundation, vice president of the Albright Knox Art Gallery Board of Directors, and a member of the board of directors for the Community Foundation for Greater Buffalo.
Delaware North is a generous benefactor of multiple non-profit institutions throughout the world, and particularly in Buffalo, NY, where they are headquartered. Delaware North has committed over $50 million to the University at Buffalo, the largest institution of the State University of New York system, and the university recently renamed its medical school the Jacobs School of Medicine and Biomedical Sciences in recognition of his family's steadfast support. Delaware North and the Jacobs family have also made $1 million donations to the Say Yes Buffalo initiative and the Explore & More Museum, both of which are committed to advancing elementary and secondary education in Buffalo.
Jacobs is past chair of the Nichols School Board of Trustees. He serves on the Say Yes Buffalo Scholarship Board, is a member of the Georgetown Board of Regents and is an active alumnus interviewer, and he served on the Georgetown College of Arts & Sciences advisory board from 1995 until 2000. Jacobs has dedicated more than a decade of volunteer service to United Way of Buffalo and Erie County, including chairing the annual fundraising campaign in 1999 and serving as chairman of the board of directors from 2003 to 2006. He currently participates on the United Way of Buffalo and Erie County Advisory Board.
Jacobs is active in numerous industry organizations including the Global Sports Summit and the U.S. Travel CEO Roundtable. He recently completed a term on the Department of Commerce's Travel and Tourism Advisory Board, which advises the Secretary of Commerce on matters related to the travel and tourism industry in the United States, including travel and tourism policies, travel facilitation and infrastructure, and the National Travel and Tourism Strategy.
The Jacobses reside in East Aurora, New York. They have two children, Melissa and Jeremy III.