There are so many neighborhoods in Atlanta that are worth exploring, you'll wish for a car to check out everything there is to do here. Local buses, while inexpensive, drop you off far from your destination. Ride hailing, like Uber or Lyft, is convenient, but rural areas may not have regular service. Plus, if you plan to go all over Johns Creek and the surrounding areas, the cost can add up.
If you want the convenience to go where you need to for an affordable rate, then you've found the best place. CarRentals.com works with the most dependable rental car businesses in the business. Hertz has over a hundred years of experience and a fleet containing several of the most well-known in the business, like Nissan and Hyundai. With Hertz's storied history and thousands of locations all over the world, you know you'll be in great hands.
How do I get a Johns Creek Hertz car rental at a great rate?
Do I need to bring anything special when I pick up my rental car in Johns Creek?
How old do I have to be to rent a car in Johns Creek?
Hertz's minimum age to rent a car is 21. Some rentals, especially higher category vehicles (luxury, SUVs, etc.), may have an added fee if you are under 25. Make sure to review Hertz's policies to know if there is an additional cost before you book.
When cruising through Johns Creek or the rest of the U.S.A., you'll need insurance. Hertz requires that you show proof of insurance before you pick up your vehicle. The majority of countries require the driver to have insurance. You might be able to purchase additional insurance through Hertz, if you know your insurance won't cover your rental. Otherwise, as a U.S. citizen, you can also purchase Collision Damage Coverage through CarRentals.com at checkout.
Many major card issuers, like Visa and MasterCard, provide some insurance on your rental, however, there are usually restrictions. For example, they may not cover your rental car if you get a larger or luxury vehicle. Make sure to check Hertz's policy before you decide.
Hertz, like many other rental car agencies, requires a deposit upon reservation. The deposit can vary greatly based on the size of the car. Furthermore, be sure you have enough funds on your credit card to make the deposit.
At CarRentals.com, we recommend a full to full policy. You pick up your Hertz rental with a full tank, and you will want to return it filled up. To avoid any added expenses, it is best to fill up your tank before bringing the vehicle to Hertz.
Why should I get unlimited miles in Johns Creek?
The majority of suppliers will offer unlimited miles, but you want to ensure it's part of the bundle. It's helpful to know how far you want to drive so you can plan your trip in advance. Although most rental car companies offer unlimited mileage, if it isn't part of your rental agreement, you could face additional cost. You may want to get unlimited miles if you are planning to discover what else Atlanta has to offer, or even the U.S. of A.
What is there to do around Johns Creek?
Once you've checked out Johns Creek, you'll be happy that you have your own vehicle. If you like to get on the greens when you are on vacation, then you've come to the right place. There are two golf courses in Atlanta. Want to work on your drives? Check out Atlanta Athletic Club or Country Club of the South. Georgia is full of things to do for tourists and locals alike. You may just have to hop into your rental car and discover what is else is out there.
With everything there is to do in Atlanta, having access to your own automobile lets you sightsee at your own pace. When you're ready to check out more of the U.S.A., you can leave when you like, without having to coordinate ride-hailing services or wait for the bus.
Heading out of town soon? Book your Hertz Johns Creek car rental and zip off to take in all the must-see sights. Go through CarRentals.com and hit the roads in Atlanta, Georgia.


Published: Apr 26, 2018 at 6 a.m.
2-4 p.m., Spring hours for the Glace Bay Heritage Museum in the Old Town Hall. Museum, Isabelle Harris Gift Shop and Second Hand Book Store will be open, 14 McKeen St., phone 902-842-5345.
7-9 p.m., Dementia/Alzheimers caregiver support group meet at Seaview Manor, 275 South St. Learn, exchange information and receive encouragement.
7 p.m., Passchendaele Al-Anon Group, Unity Club (AA room) Rear McKeen Street.
8 p.m., Island Martial Arts Centre in the lower level of the People's Mall is offering a women's only taekwondo program. Build muscle, lose weight and empower yourself.
8 p.m. Row Street Club will be hosting Loonie bullseye darts.
10-11 a.m. Tai Chi, Main-a-Dieu Coastal Discovery Centre.
6-8 p.m., Veterans' Memorial computer site is open.
11 a.m.-12 p.m., Senior Friends For Fitness class, Reserve Mines Pensioners Club Hall, Main St. Free class, everyone welcome.
8 p.m., 45s card game, Reserve Mines Seniors and Pensioners' Hall. Everyone welcome.
8 p.m., (CD) AA Reserve Midway Group meeting, St. Joseph's Church Hall, Main Street.
11 a.m.-4 p.m., Friends Quilting Group, Big Bras d'Or Firehall. Please contact Maggie 902-736-9887 or Ruth 902-674-2208.
3 p.m., Munroe Crafters Guild will meet at Boularderie School. (second Thursday of the month.
7:30 p.m., 45s card game at Southside Boularderie fire hall. Lunch served.
1:30 p.m., Northside bridge club, St. Joseph's Hall, Villa Drive.
7:30 p.m., Bras d'Or Seniors and Pensioners Club 45s card game in the hall.
5-9:30 p.m., Kitchen is open with weekly special at the North Sydney Firefighters' Club. Live entertainment goes from 6-9:30 p.m. Free admission.
7 p.m., Cribbage game, Armstrong Memorial Branch No. 19, Royal Canadian Legion.
6:30-9 p.m., 129 Caribou Sea Cadets looking for new recruits ages 12-18. Training at the Alert Building, Canadian Coast Guard College. For more information, P.J. at 902-371-6761 PJ or Pat at 902-794-7521.
6:30 p.m., Sydney Mines walking group the Walkie-Talkies will gather at the Martha Hollett Library. All ages welcome.
8 p.m., Al-Anon Harmony AFG meets at 55 King St.
8 p.m., (OS) AA Sydney Mines Group meeting, 55 King St., behind post office.


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GCWGA Foundation raises money
GCWGA club contributions should push the fundraising total past $11,000.
GCWGA Foundation raises money GCWGA club contributions should push the fundraising total past $11,000. Check out this story on cincinnati.com: http://cin.ci/1RS3Q7W
Cincinnati Published 12:40 p.m. ET Oct. 19, 2015
Warming up for the eighth annual SHE Tournament at Blue Ash Golf Course in September.(Photo: Provided)
The Greater Cincinnati Women's Golf Association Foundation hosted its eighth annual SHE Tournament in September at Blue Ash Golf Course.
Teams of four players from 22 Greater Cincinnati country clubs competed for the SHE (Scholarships for Higher Education) championship in a net two-best-ball format.
The event raised nearly $5,000 from its raffles and silent auction for prizes including golf for four at various clubs, a football signed by the Cincinnati Bengals, an autographed Marvin Lewis lithograph and more.
Coldstream Country Club took home the traveling championship trophy with a score of 127 posted by Christine Lenahan, Rita Sprenkle, Joanie Lauch and Sue Detzel.
Wetherington Country Club was runner up with a 128 carded by Sherri Pedoto, Diane Stevens, Donna Harpso and Cathy Barlow.
The SHE Tournament has raised more than $75,000 and awarded 62 scholarships since its inception in 2006.
The SHE Tournament mission is "to provide one-time awards to female high school seniors who meet a certain set of qualifications and are selected on the basis of academic achievement, excellence of character and involvement in the sport of golf."
In 2015, the GCWGA Foundation gave 10 $1,500 scholarships to area high school seniors.
"I've been part of the selection committee and it was just amazing to read what our young women do in our communities, not just on the golf course," said GCWGA Foundation member Diane Rottinghaus.
"They give a lot of hours of community service and they are all very good students. It's wonderful to be able to help these girls pursue their educations and their dreams."
Applications for the scholarships are available under the scholarship tab at the GCWGA website (www.gcwga.org) and are due March 1, 2016. Recipients will be announced in May, with the winners formally introduced and presented their checks in July.
For questions or additional information, please contact GCWGA Foundation chair Georgianne Koch at 484-6005 or scholarshipchair@gcwga.org.

redpajama_set_name: RedPajamaCommonCrawl


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Clive R Bramham
Professor, Head of Neuroscience Research Group
Bramham Lab homepage - Molecular Control of Synaptic Plasticity
E-mailClive.Bramham@uib.no
Phone+47 55 58 60 32+47 481 25 046
Department of Biomedicine
Jonas Lies vei 91
The overriding goal is to explain how information is physically stored and represented in the brain, and how these processes are disrupted, altered, or destroyed in disorders of cognition including memory loss. Our research focus is the molecular control of synaptic plasticity. We aim to uncover the logic of synaptic plasticity at the level of protein synthesis, protein functional properties, and the dynamics of protein interaction networks.
Specific research areas:
Arc as a master regulator of long-term synaptic plasticity and cognition
Translational control of synaptic plasticity
Non-coding RNA regulation and function in synaptic plasticity
Papers by topic
Hallin, E.I., Bramham, C.R., and Kursula, K. Structural properties and peptide ligand binding of the capsid homology domains of human Arc (2021) Biochem Biophys Res Commun 26, doi.org/10.1101/2020.12.17.423319
Eriksen MS, Nikolaienko O, Hallin EI, Grødem S, Bustad HJ, Flydal MI, Merski I, Hosokawa T, Lascu D, Akerkar S, Cuéllar J, Chambers JJ, O'Connell R, Muruganandam G, Loris R, Touma C, Kanhema T, Hayashi Y, Stratton MM, Valpuesta JM, Kursula P, Martinez A and Bramham CR (2020). Arc self-association and formation of virus-like capsids are mediated by an N-terminal helical coil motif. The FEBS Journal. https://doi.org/10.1111/febs.15618
Zhang, H. and Bramham, C.R. (2020) Arc function in long-term synaptic plasticity: emerging mechanisms and unresolved issues. Eur J Neurosci, doi.org/10.1111/ejn.14958
Hallin, EI, Eriksen, M., Baryshnikov, S., Nikolaienko, Grødem, S., Hosokawa, Y. Hayashi, Y., *Bramham, C.R. and *Kursula, P. (2018) Structure of monomeric full-length ARC sheds light on molecular flexibility, protein interactions, and functional modalities. J. Neurochem. doi.org/10.1111/jnc.14556.
Nikolaienko, O., Patil, S, Eriksen, M.S., and Bramham, C.R., (2018) Arc protein: a flexible hub for synaptic plasticity and cognition. Semin Cell Dev Biol, 77:33-42. dx.doi.org/10.1016/j.semcdb.2017.09.006
Nair, R.R., Patil S., Tiron, A, Kanhema, T., Panja, D., Schiro, L., Parobzak, K., Wilczynski, G., and Bramham, C.R. (2017) Dynamic Arc SUMOylation and selective interaction with F-actin binding protein drebrin A in LTP consolidation in vivo. Front Synaptic Neurosci. doi: 10.3389/fnsyn.2017.00008
Gozdz, A., Nikolaienko, O., Urbanska, M., Cymerman, I.A., Sitkiewicz, E., Dadlez, M., Bramham. C.R., and Jaworski, J (2017) GSK3α and GSK3β phosphorylate Arc and regulate its degradation. Front Mol Neurosci. http://doi: 10.3389/fnmol.2017.00192
Nikolaienko O, Eriksen MS, Patil S, Bito H, and Bramham CR (2017) Stimulus-evoked ERK-dependent phosphorylation of activity-regulated cytoskeleton-associated protein (Arc) regulates its neuronal subcellular localization. Neuroscience 360:68–80. http://doi: 10.1016/j.neuroscience.2017.07.026.
Myrum, C., Soulé, J., Bittins, M., Cavagnini, K., Eriksen, M.S., Goff, K., Ziemek, S., Patil, S., Szum, A., Nair, R.R. and Bramham, C.R. (2017) Arc interacts with the integral ER protein, calnexin. Frontiers Cell Neurosci. doi.org/10.3389/fncel.2017.00294.
Kuipers, S., Trentani, A., Tiron, A, Mao, X., Kuhl, D., and Bramham, C.R. (2016) BDNF-induced LTP is associated with rapid Arc-dependent enhancement in adult hippocampal neurogenesis. Scientific Reports, http://doi: 10.1038/srep21222.
Myrum,C., Baumann, A., Bustad, H.J., Flydal, M.I., Mariaule,V., Alvira, S., Cuéllar, J., Soulé, J., Valpuesta J.M., Márquez, J.A., *Martinez, A., and *Bramham,C.R. (2015) Arc is a flexible modular protein capable of reversible self-oligomerization. Biochem J. 468, 145-158. http://doi 10.1042/BJ20141446
Myrum C, Giddaluru S, Jacobsen K, Espeseth T, Nyberg L, Lundervold A J, Haavik J, Nilsson L, Reinvang I, Steen V M, Johansson S, Wibrand K, *Le Hellard S, and *Bramham C R. (2015) Common variants in the ARC gene are not associated with cognitive abilities. Brain and Behavior, doi: 10.1002/brb3.376.
Soule J, Alme MN, Myrum C, Schubert M, Kanhema T, Bramham CR (2012) Balancing Arc synthesis, mRNA decay, and proteasomal degradation: maximal protein expression triggered by REM sleep-like bursts of muscarinic cholinergic receptor stimulation. J Biological Chemistry, 287(26): 22354-66.
Wibrand, K., Pai, B., Siripornmongcolchai, T, Bittins, M., Berentsen, B., Ofte, M.L, Weigel, A., Skaftnesmo, K.O., and Bramham C.R. (2012) MicroRNA regulation of the synaptic plasticity related gene Arc. PLoS ONE 7(7): e41688.
Bramham CR, Alme MN, Bittins M, Kuipers SD, Nair RR, Pai B, Panja D, Schubert M, Soule J, Tiron A, Wibrand K (2010) The Arc of synaptic memory. Exp Brain Res 200:125-140.
Kuipers SD, Tiron A, Soule J, Messaoudi E, Trentani A, Bramham CR (2009) Selective survival and maturation of adult-born dentate granule cells expressing the immediate early gene Arc/Arg3.1. PLoS ONE 4(3): e4885.
Bramham CR, Worley PF, Moore MJ, Guzowski JF (2008) The immediate early gene Arc/Arg.1: regulation, mechanisms, and function. J Neurosci. 27(39): 10445-10455.
Soule J, Penke-Verdier Z, Alme M, Kanhema T, Laroche S, Bramham CR (2008) Object-place recognition learning triggers rapid induction of plasticity-related immediate early genes and synaptic proteins in the rat dentate gyrus. Neural Plasticity, Article ID 269097, 12 pages.
Messaoudi,E., Kanhema,T., Soule,J., Tiron,A., Dagyte,G., da Silva,B., and Bramham,C.R. (2007) Sustained Arc synthesis controls LTP consolidation through regulation of local actin polymerization in the dentate gyrus in vivo. J. Neurosci. 27: 10445-10455.
Ying SW, Futter M, Rosenblum K, Webber MJ, Hunt SP, Bliss TV, Bramham CR (2002) Brain-derived neurotrophic factor induces long-term potentiation in intact adult hippocampus: requirement for ERK activation coupled to CREB and upregulation of Arc synthesis. J Neurosci 22: 1532-1540.
BDNF
Cassarotto, P., Girych, M., Fred, S.M., Moliner, R., Enkavi, G., Biojone, C., Cannarozzo, C., Brunello, C.A, Steinzeig, A., Winkel, F., Patil, S., Vestring, S., Serchov, T., Laukkanen, L., Cardon, I., Antila, H., Rog, T., Bramham, C.R., Normann, C., Lauri, S.E., Vattulainen, I., and Castrén, E., (2021) Antidepressants act by directly binding to TRKB neurotrophin receptors. Cell 184:1-15. 10.1016/j.cell.2021.01.034
Esvald, E.-E., Tuvikene, J., Sirp, A., Patil, S., Bramham, C.R., & Timmusk, T. (2020) CREB family transcription factors are major mediators of BDNF transcriptional autoregulation in cortical neurons. J. Neurosci., 40(7):1405-1426. doi.org/10.1523/JNEUROSCI.0367-19.2019.
Panja, D and Bramham, C.R. (2017) BDNF function in long-term synaptic plasticity in the dentate gyrus in vivo: methods for local drug delivery and biochemical analysis of translation. In: Neuromethods. Humana Press. doi.org/10.1007/7657_2017_7
Kuipers, S., Trentani, A., Tiron, A, Mao, X., Kuhl, D., and Bramham, C.R. (2016) BDNF-induced LTP is associated with rapid Arc-dependent enhancement in adult hippocampal neurogenesis. Scientific Reports, doi: 10.1038/srep21222.
Panja, D., Kenney, J.W., D'Andrea, L., Zalfa, F., Vedeler, A., Wibrand, K., Fukunaga, R., Bagni, C., Proud, C.G., and Bramham, C.R. (2014). Two-stage translational control of dentate gyrus LTP consolidation is mediated by sustained BDNF-TrkB signaling to MNK. Cell Rep. 9, 1430–1445.
Panja, D., and Bramham, C. R. (2014). BDNF mechanisms in late LTP formation: a synthesis and breakdown. Neuropharmacology, 76: 664-676 . doi:10.1016/j.neuropharm.2013.06.024
Coppens, C. M., Siripornmongcolchai, T., Wibrand, K., Alme, M. N., Buwalda, B., de Boer, S. F., Koolhaas, J. M., and Bramham, C. R. (2011) Social defeat during adolescence and adulthood differentially induce BDNF-regulated immediate early genes. Front Behav. Neurosci. 5:72., Epub Nov 2.
Alme MN, Wibrand K, Dagestad G, Bramham CR (2007) Chronic fluoxetine treatment induces brain region-specific upregulation of genes associated with BDNF-induced long-term potentiation. Neural Plast 2007: 26496. PMID: 18301726
Wibrand K, Messaoudi E, Havik B, Steenslid V, Løvlie R, Steen VM, and Bramham CR (2006) Identification of genes co-upregulated with Arc during BDNF-induced long-term potentiation in the adult rat dentate gyrus in vivo. Eur J Neurosci 23: 1501-1511.
Kanhema, T., Dagestad, G., Panja, D., Messaoudi, E., Haavik, B., Ying, S.W., Nairn, A.C., Sonenberg, N. and Bramham, C.R. (2006) Dual regulation of translation initiation and peptide chain elongation during BDNF-induced LTP in vivo: evidence for compartment-specific translation control. J Neurochem. 99:1328-1337.
Bramham,C.R and Messaoudi, E. (2005) BDNF function in adult synaptic plasticity: the synaptic consolidation hypothesis. Prog. Neurobiol, 76: 99-125.
Gooney, M., Messaoudi, E., Maher, F.O., *Bramham, C.R., and *Lynch, M.A. (2004) BDNF-induced LTP in dentate gyrus is impaired with age: analysis of changes in cell signalling events. Neurbiol Aging. 25: 1323-1331.
Messaoudi E, Ying SW, Kanhema T, Croll SD, Bramham CR (2002) BDNF triggers transcription-dependent, late phase LTP in vivo. J Neurosci 22: 7453-7461.
Messaoudi, E., Bårdsen, K., Srebro, B., and C.R. Bramham (1998) Acute intrahippocampal infusion of brain-derived neurotrophic factor induces lasting potentiation of synaptic transmission in the rat dentate gyrus. J. Neurophysiol. 79: 496-499.
Translational control and dendritic protein synthesis
Chalkiadaki, K., Kouloulia, S., Bramham, C.R., and Gkogkas, C (2020) Regulation of protein synthesis by eIF4E in the brain. In The Oxford Handbook of Neuronal Protein Synthesis pp 1–22. 10.1093/oxfordhb/9780190686307.013.12
Taha E, Patil S, Barrera I, Proud CG, Bramham CR, Rosenblum K (2020) eEF2/eEF2K pathway in the mature dentate gyrus determines neurogenesis level and cognition. Current Biology 30:1–15. doi.org/10.1016/j.cub.2020.06.061.
Berentsen B, Patil S, Wibrand K, Goff KM, Pajak M, Simpson IT, and Bramham CR. (2020) microRNA-34a acutely regulates synaptic efficacy in the adult dentate gyrus in vivo. Molecular Neurobiology doi.org/10.1007/s12035-019-01816-1
Bramham, C.R., Jensen, K, and Proud, CG. (2016) Tuning specific translation in cancer metastasis and synaptic memory: control at the MNK-eIF4E axis. Trends in Biochemistry, 41: 847-858. dx.doi.org/10.1016/j.tibs.2016.07.008.
Grønli, J., Soulé, J., and Bramham, C.R. (2014). Sleep and protein synthesis-dependent synaptic plasticity: impacts of sleep loss and stress. Front. Behav. Neurosci. 7, 1–18.
Grønli,J., Dagestad,G., Milde,A.M., Murison,R., and Bramham,C.R. (2012). Post-transcriptional effects and interactions between chronic mild stress and acute sleep deprivation: Regulation of translation factor and cytoplasmic polyadenylation element-binding protein phosphorylation. Behav. Brain Res. 235, 251-262.
Panja, D., Dagyte, G., Bidinosti, M.,. Wibrand, K., Kristiansen, A.M., Sonenberg, N., and Bramham, C.R. (2009) Novel translational control in Arc-dependent long-term potentiation consolidation in vivo. J. Biological Chemistry 284: 31498-31511.
Bramham, C.R. (2008) Local protein synthesis, actin dynamics, and LTP consolidation. Curr Opin Neurobiol. 18: 524-531.
Bramham C. R. and Wells D. G. (2007) Dendritic mRNA: transport, translation, and function. Nature Rev Neurosci, 8 (10):776 – 789.
Dagestad,G., Messaoudi,E., and Bramham,C.R. (2006). Chronic fluoxetine induces region specific changes in translation factor eIF4E and eEF2 activity in the rat brain. Eur J Neurosci., 23: 2814-2818.
Håvik, B., Røkke, H., Bårdsen, K., Davanger, S. and Bramham, C.R. (2003) High-frequency bursts trigger rapid delivery of pre-existing CaMKII mRNA to synapses: a mechanism in dendritic protein synthesis during long-term potentiation in adult awake rats. Eur. J. Neurosci., 17: 2679-2689.
Gene expression and non-coding RNAs
Maag, J.L.V. Panja, D, Kaczorowski, D.C. Peters, T.J., Bramham, C.R., Wibrand, K., and Dinger, M.E. (2017) Widespread promoter methylation of synaptic plasticity genes in long-term potentiation in the adult brain in vivo. BMC Genomics. 18 (2017) 250. doi:10.1186/s12864-017-3621-x.
Maag, J.L.V., Panja,D., Sporild, I, Patil, S., Kaczorowski, D.C., *Bramham, C.R., *Dinger, M., and *Wibrand, K. (2015) Dynamic expression of long noncoding RNAs and repeat elements in synaptic plasticity. Frontiers in Neuroscience. 9:351. doi:10.3389/fnins.2015.00351
Pai, B., Siripornmongcolchai, T., Berentsen, B., Pakzad, A., Vieuille, C., Pallesen, S., Pajak, M., Simpson, T.I., Armstrong, J.D., Wibrand, K., and Bramham, C.R. (2014). NMDA receptor-dependent regulation of miRNA expression and association with Argonaute during LTP in vivo. Front. Cell. Neurosci. 7, 1–15.
Wibrand, K., Panja, D., Tiron, A., Ofte, M.L., Skaftnesmo, K. Sohn-Lee, C., Pena, J., Tuschl, T. and Bramham, C.R. (2010) Differential regulation of mature and precursor microRNA expression by NMDAR and metabotropic glutamate receptor expression activation during LTP in the dentate gyrus in vivo. Eur J Neurosci 31: 636-645.
Håvik, B., Røkke, H., Dagyte, G., Stavrum, A-K., *Bramham, C.R., and *Steen, V.M. (2007) Synaptic activity-induced global gene expression patterns in the dentate gyrus of adult behaving rats: induction of immunity-linked gene sets. (*Equal contribution). Neuroscience, 148: 925-936.
Myrum, C., Nikolaienko, O. Bramham, C.R. Haavik, J., and Zayats, T. Implication of the APP gene in intellectual abilities. (2017) J Alz Dis. 59(2):723-735. doi: 10.3233/JAD-170049.
Havik, B., Degenhardt, F. A., Johansson, S., Fernandes, C. P., Hinney, A., Scherag, A., Lybaek, H., Djurovic, S., Christoforou, A., Ersland, K. M., Giddaluru, S., O'Donovan, M. C., Owen, M. J., Craddock, N., Muhleisen, T. W., Mattheisen, M., Schimmelmann, B. G., Renner, T., Warnke, A., Herpertz-Dahlmann, B., Sinzig, J., Albayrak, O., Rietschel, M., Nothen, M. M., Bramham, C. R., Werge, T., Hebebrand, J., Haavik, J., Andreassen, O. A., Cichon, S., Steen, V. M., and Le Hellard S. (2012) DCLK1 Variants are associated across schizophrenia and attention deficit/hyperactivity disorder PLoS ONE 7, e35424
Le Hellard S, Havik B, Espeseth T, Breilid H, Lovlie R, Luciano M, Gow AJ, Harris SE, Starr JM, Wibrand K, Lundervold AJ, Porteous DJ, Bramham CR, Deary IJ, Reinvang I, Steen VM (2009) Variants in doublecortin- and calmodulin kinase like 1, a gene up-regulated by BDNF, are associated with memory and general cognitive abilities. PLoS One 4:e7534.
Publications in CRIStin database with links:
Show author(s) (2020). eEF2/eEF2K Pathway in the Mature Dentate Gyrus Determines Neurogenesis Level and Cognition. Current Biology. 3507-3521.
Show author(s) (2020). The solution structure of the human brain-protein arc studied by NMR.
Show author(s) (2020). Investigation of Arc interaction with mRNA in the nucleus of SH-SY5Y Neuroblastoma cells.
Show author(s) (2020). Cognitive function and brain plasticity in a rat model of shift work: role of daily rhythms, sleep and glucocorticoids. Scientific Reports.
Show author(s) (2020). CREB family transcription factors are major mediators of BDNF transcriptional autoregulation in cortical neurons. Journal of Neuroscience. 1405-1426.
Show author(s) (2020). Bidirectional Dysregulation of AMPA Receptor-Mediated Synaptic Transmission and Plasticity in Brain Disorders. Frontiers in Synaptic Neuroscience.
Show author(s) (2020). Arc/Arg3.1 function in long-term synaptic plasticity: Emerging mechanisms and unresolved issues. European Journal of Neuroscience.
Show author(s) (2020). Arc self‐association and formation of virus‐like capsids are mediated by an N‐terminal helical coil motif. The FEBS Journal.
Show author(s) (2019). MicroRNA-34a acutely regulates synaptic efficacy in the adult dentate gyrus in vivo. Molecular Neurobiology. 1-14.
Show author(s) (2019). A simple DMSO-based method for cryopreservation of primary hippocampal and cortical neurons. Journal of Neuroscience Methods.
Show author(s) (2018). The immediate early protein Arc: an exploration of protein structure and regulation.
Show author(s) (2018). Structure of monomeric full‐length ARC sheds light on molecular flexibility, protein interactions, and functional modalities. Journal of Neurochemistry. 323-343.
Show author(s) (2018). Extending the photoperiod impacts circadian rhythmicity and gene expression in prefrontal cortex and retina- Impact of exposure to blue-enriched light. .
Show author(s) (2018). Extended photoperiod alters sleep and expression of synaptic plasticity-associated genes. The impact of blue-enriched light.
Show author(s) (2018). Extended photoperiod alters circadian rhythmicity and expression of neuroplasticity markers. The impact of blue-enriched light.
Show author(s) (2017). Widespread promoter methylation of synaptic plasticity genes in long-term potentiation in the adult brain in vivo. BMC Genomics.
Show author(s) (2017). The RNA-Binding Protein hnRNP K Mediates the Effect of BDNF on Dendritic mRNA Metabolism and Regulates Synaptic NMDA Receptors in Hippocampal Neurons. eNeuro.
Show author(s) (2017). Stimulus-evoked ERK-dependent phosphorylation of activity-regulated cytoskeleton-associated protein (Arc) regulates its neuronal subcellular localization. Neuroscience. 68-80.
Show author(s) (2017). No escaping the rat race: simulated night shift work alters the time-of-day variation in BMAL1 translational activity in the prefrontal cortex. Frontiers in Neural Circuits. 1-12.
Show author(s) (2017). Implication of the APP gene in intellectual abilities. Journal of Alzheimer's Disease. 723-735.
Show author(s) (2017). GSK3α and GSK3β Phosphorylate Arc and Regulate its Degradation. Frontiers in Molecular Neuroscience.
Show author(s) (2017). Dynamics of actin cytoskeleton in dendritic spines -interactions between Arc and Drebrin A.
Show author(s) (2017). Dynamic Arc SUMOylation and selective interaction with F-actin-binding protein Drebrin A in LTP consolidation in vivo. Frontiers in Synaptic Neuroscience. 1-|14.
Show author(s) (2017). Dynamic Analysis of Arc Protein Oligomerization by Förster Resonance Energy Transfer.
Show author(s) (2017). Arc protein: a flexible hub for synaptic plasticity and cognition. Seminars in Cell and Developmental Biology. 33-42.
Show author(s) (2017). Arc interacts with the integral endoplasmic reticulum protein, calnexin. Frontiers in Cellular Neuroscience. 1-12.
Show author(s) (2017). Arc expression and protein-protein interactions in a mouse model of Alzheimer's disease: Exercise- and novelty-induced changes in Arc, BDNF, and PS1 expression and Arc PS1 interaction in APP/PS1 and WT mice.
Show author(s) (2017). Activity-Regulated Cytoskeleton-associated (Arc) Protein: Interaction with Actin-Binding Proteins in the adult rat brain.
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More information in national current research information system (CRIStin)
Arc as a master regulator of long-term synaptic plasticity
Links to currently funded projects:t
The Impact of Cytoplasmic Polyadenylation on Local Translation in Neurons. EEA grant for Poland-Norway Research Cooperation. 2020-2024.
Mohn Research Center for Plasticity and Neural Circuit Dynamics in the Brain. Supported by the Trond Mohn Foundation, the University of Bergen (UiB) and the Norwegian University of Science and Technology (NTNU). 2021-2026.
In vivo electrophysiological studies of synaptic plasticity combined with genetic and local pharmacological manipulations.
Live-cell imaging in primary neuronal cultures, brain tissue slices, and intact rodents. Two-photon laser-scanning microscopy. FRET imaging and single-particle tracking. Single-cell electroporation.
Biochemical analysis of signal transduction mechanisms, protein-protein interactions, and functional analysis of post-translational modifications.
Live-cell microscopy
Neuropsychiatry
Synaptic Plasticity
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By Harvard Medical International
Thu 12 Jun 2008 04:00 AM
Partners Harvard Medical International (PHMI)
Treating prostate cancer
A look at the pros and cons of PSA screening and the treatment options available for prostate cancer.
According to the American Cancer Society, about 186,320 Americans will be diagnosed with prostate cancer this year, and 28,660 will die from the disease.
That makes prostate cancer the most common internal malignancy in American men, with a cancer death toll that trails only lung cancer.
Researchers have made substantial progress in understanding the causes and basic biology of the disease, and clinicians have developed improved methods of diagnosis and therapy.
Dietary fat — particularly saturated fat from animal products — appears to fuel the disease.
Even so, basic questions remain unanswered; as a result, many important decisions about prostate cancer are not made by doctors but by patients.
The first decision a man faces is whether or not to have a blood prostate-specific antigen (PSA) test and a digital rectal exam (DRE) to screen for early prostate cancer. Although many men find the decision difficult, there is no wrong answer.
Proponents of screening point out that PSA testing is the best way to diagnose prostate cancer in its earliest, most treatable stages. Sceptics counter that some men diagnosed by screening receive treatments that produce more ill effects than the disease itself. Odd as it sounds, both sides are right.
That's why Harvard Men's Health Watch has not taken a position on PSA screening; instead, we've tried to explain the pros and cons so each man can decide what's best for him.
In fact, informed decision-making is the approach recommended by every major medical organization that has weighed in on the question, ranging from the American Cancer Society and the American Urological Association to the American College of Physicians and the American Academy of Family Physicians.
Once a man is diagnosed with prostate cancer, his decisions take on a new urgency. In the case of most malignancies, news of the diagnosis is accompanied by a crisp and confident treatment plan.
Not so with prostate cancer; instead, the doctor who announces the diagnosis is likely to ask the patient what treatment he wants.
That means the shock of a diagnosis is followed by the shock of learning that, in many cases, doctors disagree about which treatment is best.
It's not that doctors haven't tried to answer the question themselves. In 1995 and again in 2007 the American Urological Association published reports by the authoritative Prostate Cancer Clinical Guidelines Panel.
In both cases, dozens of experts reviewed thousands of studies but were unable to establish standard-of-care recommendations.
Instead, the experts recognized that there are many acceptable therapeutic options, and they suggested that doctors inform their patients about the advantages and disadvantages of each treatment, enabling every man to choose for himself.
And a major 2008 review sponsored by the U.S. Agency for Healthcare Research and Quality agreed, concluding that "Assessment of the comparative effectiveness and harms of localized prostate cancer treatments is difficult because of lack of evidence.
Let's examine why prostate cancer is different from other malignancies, and what makes studies hard to perform and tricky to interpret.
The natural history of prostate cancer
Scientists don't know how prostate cancer gets started or what causes it, but several factors are important. Genetics certainly play a role.
Men with fathers or brothers who've had prostate cancer are 1.5 to 3 times more likely to get the disease than men with no family history, and if multiple relatives have been diagnosed before age 55, a man's risk rises even further.Hormones also play a role; testosterone and other androgens (male hormones) stimulate the growth of prostate cells, both benign and malignant, but there is no simple link between testosterone levels and risk. Lifestyle is also important.
Prostate cancer is vastly more common in white Americans than in Japanese or Chinese men - but when Asians move to the U.S. and adopt Western habits, they quickly acquire the high risk of native-born Americans.
Diet is the most important lifestyle risk factor. Dietary fat - particularly saturated fat from animal products - appears to fuel the disease, and very high levels of calcium and alpha-linolenic acid (the omega-3 fat in flaxseeds and canola oil) may also have an adverse effect.
In contrast, tomatoes and other vegetables, soy products, fish, and whole grains may be protective. Obesity increases risk. And although the evidence is mixed, exercise may be helpful, smoking harmful. Though factors contribute to prostate cancer, they act slowly.
That's why age is the greatest predictor of risk.
It's a bit scary: if you live long enough, you probably will get prostate cancer. Remember, though, that most of the prostate cancers in these surveys are clinically unimportant - a few malignant cells discovered in the course of complete autopsies on men who died from other causes.
In all, an American man's lifetime risk of developing early microscopic prostate cancer is at least 30%, but his risk of clinically diagnosed prostate cancer is only about 16%.
A one-in-six chance of being diagnosed with prostate cancer is scary, but a white American's risk of dying from the disease is only about 3%, an African American's, about twice that.
Why the debate?
In most forms of cancer, diagnosis and treatment go hand in hand; it may be hard for a doctor to diagnose a tumor, but once he knows it's there, he can offer a clear plan of treatment based on solid scientific evidence that's backed by experts. Why is prostate cancer so different?
First, the disease is different. Most cancers behave predictably, but prostate cancer does not; sometimes it's aggressive and dangerous, but often it's indolent or even harmless.
Second, the cancer grows slowly. With many malignancies, a five-year survival is tantamount to cure, so clinical trials can learn if a treatment is effective in a relatively short time. But most patients with prostate cancer survive for more than five years with any form of treatment - or with no treatment at all.
An important 1995 study found that most cases remain indolent for 10 to 15 years after diagnosis, even without therapy.
After that, however, the prostate cancer death rate triples. As a result, it may take 10 or 15 years for a study to learn how well a treatment works.
Third, the diagnosis of prostate cancer has changed dramatically. Before 1992, the disease was most often discovered as the result of a DRE or a pathological examination of tissue obtained during a transurethral resection of the prostate (TURP), performed to treat benign prostatic hyperplasia (BPH).
At present, prostate cancer is most often diagnosed as the result of a PSA blood test.
Widespread PSA testing has produced an explosive rise in the number of cases detected, particularly in young men with early disease. Doctors don't yet know if the cancers detected by PSA screening will behave the same way as the cancers detected by older methods.
Fourth, the treatment is also changing. For many years, the options for active therapy were limited to surgery, external beam radiation, and hormonal therapy.
Doctors have developed greatly improved techniques for each of these standard treatments - and they have also developed entirely new approaches, such as brachytherapy with implanted radioactive seeds; cryotherapy, which kills prostate cells by freezing them; and neoadjuvant therapy, which combines radiation with hormone treatment. It is heartening, but these advances make a man's decisions even more complex.
Finally, and most importantly, only a tiny number of solid scientific trials that compare treatment options have been completed.
When the American Urological Association tried to compare the outcome of patients treated with active surveillance, surgery, or radiation, they found they were comparing apples to oranges.
The vast majority of studies that have been completed to date differ so substantially in patient age, disease stage, and follow-up that comparisons are not possible.
New studies to resolve these issues are already in progress, but until the results are in, the only option is to consider each treatment on its own merits. Tricky statistics
Doctors know that prostate cancer is a complex and puzzling disease. They also know that the only way to get answers is with scientific study. Thousands of studies of prostate cancer have been published and many more are under way.
A great deal has been learned, but many reports contain biases that are overlooked by the media, and even by some experts who cite them to argue for one interpretation or another. Perhaps that's why Mark Twain said, "There are lies, damned lies, and statistics.
Medical statistics is a complex field, and few of us aspire to expertise. Still, you may wish to consider the three most common flaws that are often overlooked in interpreting studies of prostate cancer diagnosis and treatments.
Lead-time bias To understand this, suppose that Joe and Jim are identical twins who maintained identical health habits throughout life. At age 50, Joe decided to accept annual PSA screening but Jim did not. At 60, Joe was found to have prostate cancer.
He underwent a radical prostatectomy, but his disease recurred at age 70, and he died at 75. Meanwhile Jim felt fine until age 70, when bone pain led to a diagnosis of widespread prostate cancer. He improved with hormone treatment but died at age 75.
Comparing the two brothers, early diagnosis and treatment appears the winner, producing 15 years of survival after diagnosis versus just five years for delayed diagnosis and treatment.
In fact, though, both men had the same life expectancy and fate. The only thing that appears to favor Joe is earlier diagnosis; that difference is lead-time bias.
Length-time bias Slow-growing cancers are likely to be clinically silent and to be diagnosed by screening. But aggressive tumors are more likely to produce symptoms and to be diagnosed because of those symptoms.
As a result, a higher proportion of cancers detected today by PSA screening are indolent, while a higher proportion of cancers that were diagnosed in the past only after they produced symptoms were likely to be aggressive.
That makes it hazardous to compare disease-free survival rates in the PSA era with those in unscreened populations; the apparent improvements in the PSA era could be explained by length-time bias.
In Facts and Figures 2006, the American Cancer Society states that the five-year survival rates for all stages of prostate cancer have increased since the late 1980s, from 67% in the pre-PSA era to nearly 100% now.
It's always nice to announce good news, but how would you interpret this statement? Is it a tribute to early diagnosis and better treatment, or the result of comparing apples to oranges? Progress or bias - or can we tell? And is five-year survival a good benchmark for prostate cancer?
Selection bias In many studies, prostate cancer patients who are treated surgically tend to be younger and to have earlier disease and better overall health than patients who receive radiotherapy.
Similarly, patients who are observed without treatment tend to be older and to have poorer general health. These differences produce selection bias that can muddy comparisons between various types of treatment.
The only way to fully overcome selection bias is to study patients who agree to be randomly assigned to one treatment or another. To date, only one modern, randomized clinical trial that compared prostate cancer therapy to observation has been published.
This important study showed that surgery was superior to watchful waiting, at least for some men.
No rush to judgment
A diagnosis of cancer is always frightening. Men who receive a diagnosis of early prostate cancer are faced with a choice between active surveillance without immediate therapy, or surgery, radiation, and, in some centres, cryotherapy.
Many men feel pressed to decide quickly so they can get on with treatment. Fortunately, careful studies show that because prostate cancer grows slowly, treatment can be delayed for many months without harm.
Since there is no need to rush into treatment, men should take the time they need to gather information, digest the facts, and discuss options with relatives and friends. Because sexual function may be influenced by treatment decisions, a man's spouse or partner should always participate in these decisions.
In many cases, the decision-making process will benefit from independent second and third opinions from doctors with different perspectives; urologists, radiation oncologists, and medical oncologists have their own views, and each can help.
A diagnosis of prostate cancer calls for difficult decisions, but they should never be rushed or made alone.
This article is provided courtesy of Harvard Medical International. © 2008 President and Fellows of Harvard College.
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Gypsum is a soft, pale, calcium-based mineral. When used in masonry and other construction work, it is often called plaster of Paris. Gypsum dissolves easily in a warm solution of dilute hydrochloric acid. Researchers use this method to dissolve gypsum in soils when the mineral is getting in the way of their soil research.
Put the soil sample in the beaker, and add 25 millileters of 2M hydrogen chloride.
Add 500 millileters of water.
Use the electric stirrer on the mixture for a full hour. Allow it to clear and decant. Sparse crystals of gypsum should appear on the sides of the beaker.
Continue shaking and decanting until no further gypsum crystals can be seen.
Hydrochloric acid is a corrosive agent. Always wear protection for your eyes and hands when handling it.
J.D. Richards has worked as a writer and journalist since 2005. He has written for various publications, including the alt-weekly "Creative Loafing" in Florida as well as Manhattan's "New York Press" and "Blackbook Magazine." He graduated from the University of Florida with a Bachelor of Science in journalism.


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Scenic Dorset route that offers stunning coastal views and feels like a rollercoaster
With gentle bends and sea views, it's easy to see why it's so popular
The B3157 Coast Road outside of Portesham, Dorset (Image: Reach PLC)
It's fair to say that there are many great roads to drive on in Dorset.
You have the scenic A37 that takes in high views of rural Dorset, the A350 which takes you past National Trust's Melbury Downs or the A353 through Osmington which offers amazing sea views.
But one road in particular reminds you of how beautiful Dorset really is and offers such an enjoyable driving experience.
Read more: One in seven speeding tickets are cancelled in Dorset - with most people being 'caught on camera'
The B3157 Coast Road, which takes approximately 35 minutes to complete, runs all the way from Weymouth to Bridport area and offers a driving experience you won't forget.
With curved roads and glorious views of the Jurassic Coast and surrounding Dorset countryside, it's a route popular with tourists and bikers as they calmly navigate the road's various bends.
It has to be made clear that there is a speed limit that strongly needs to be adhered to and motorists should not get lost in the moment and think they are Lewis Hamilton.
The Coast Road takes motorists through villages full of picturequese and quintessential English charm and character, namely Abbotsbury, Burton Bradstock and Portesham.
The B3157 Coast Road in Dorset (Image: Reach PLC)
For motorists travelling from Weymouth, Portesham is the first village motorists will encounter.
Drivers can stop here for a drink or bite at the Duck's Farm Shop and Cafe, have a pub lunch at The Kings Arms or take a detour to Hardy's monument.
From here, you will get a glimpse of the green Dorset countryside and what to expect as you tackle the route's gentle bends.
The next village of Abbotsbury is a picture-postcard area which is home to the famous Swannery and St Catherine's Chapel and boasts tremendous views along Chesil Beach and the Jurassic Coast. Houses here are highly sought after and it's easy to see why.
As motorists exit Abbotsbury, drivers have their first sight of Chesil Beach from the road near to Abbotsbury Gardens.
Then there's Abbotsbury Hill, which tests a drivers' clutch control and use of their gears as they climb up the road.
The view from Abbotsbury Hill (Image: Google)
It is far too common to be stuck behind a vehicle struggling to go above 35mph on this 50mph stretch of road because the driver cannot effectively change gear.
But at least motorists can take in more coastal views, fields of livestock grazing and eating grass at a more leisurely pace.
The further drivers climb up Abbotsbury, the more they will see of Chesil Beach and the historic Jurassic Coast.
There are several laybys where you can pull in to get a photo of the Fleet and Chesil Beach or to enjoy a car picnic while overlooking the stunning views.
I would highly recommend this on a summer's day as you see the sunshine light up the sea.
Upon hitting the Coast Road's peak, it's all downhill from here in a literal sense - but the driving experiences keep coming.
With blind bends and hidden dips, it starts to feel like a rollercoaster as your vehicle hugs the corners of the route and within the white lines.
This does however mean drivers must remain alert, drive carefully and of course not exceed the speed limit.
A brief look at court listings at Weymouth Magistrates' Court throws up the odd driver caught speeding on the Coast Road, as police officers like to monitor peoples' driving behaviour on this favoured West Dorset route.
After Abbotsbury Hill are uninterrupted views of the sea and a clear sign that you're nearly at the scenic Hive Beach in Burton Bradstock or can get a glimpse of West Bay.
A few miles later is the village of Swyre. As the speed limit drops to 30mph, you can pull in for a pit stop at the Bull Inn, Vurlands Animal Farm for some family fun or visit the popular Manor House.
Beyond Swyre, the road climbs again and the coastal views remind you that Bridport is getting even closer.
(Image: Google)
At one point you can see the historic village of Burton Bradstock, which boasts scenic sea views, traditional tearooms and an excellent seafood restaurant to visit.
Further down the route you can take a right and visit the popular Parlour restaurant, which is a farmland restaurant that has won rave reviews from national food critics.
After driving through Burton Bradstock, you can either take a left to Station Road and West Bay, or continue on the road to travel to Bridport.
Either destination will offer something for you, whether it be a fish and chips and beach walk at West Bay or a visit to an historic market town that offers plenty of independent shops to browse in.
It's no wonder that the route consistently gains recognition for being among the country's most scenic routes given its fun but gentle bends, its various dips but the breathtaking views of the Jurassic Coast.
If you haven't tried the 18-mile route yet, it's definitely worth your time and fuel.
Do you have a story that you would like us to look into? Let us know at news.dorsetlive@reachplc.com
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When Dorset is set to host Tour of Britain for first time
We spent an hour in the road infamous for being a 'rat-run' and this is what happened


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Rick Rhoden
Sport: Golf
Team: Albuquerque
School: Atlantic High School
Richard Alan Rhoden was born on May 16, 1953 in Boynton Beach, FL. Overcoming a childhood bone disease called osteomyelitis, he attended Atlantic High School in Delray Beach. There, he became the star pitcher for the school's baseball team. Instead of attending college in 1971 after graduation, Rhoden elected to play minor league baseball.
From 1971 to 1974, he played minor league baseball for Daytona Beach, El Paso, and Albuquerque. In 1974, he was called up to the majors by the Los Angeles Dodgers on July 5th. From there, he played for the Pittsburgh Pirates, the New York Yankees, and the Houston Astros. His final game was with the Astros on September 29, 1989. During his baseball career, Rhoden batted .238 with nine home runs and 75 RBI. His career highlights were: two-time All-Star selection (1976, 1986) and three-time Silver Slugger Award (1984, 1985, 1986).
Since his retirement from baseball, Rhoden has picked up a new professional sport – golf. Qualifying for the U.S. Senior Open and becoming a dominant player of the Celebrity Players Tour, he has played in a number of Champions Tour events. Rhoden has won the American Century Celebrity Golf Classic eight times.


wide a berth as possible; and especially when she was to windward and therefore far safer. Only someone prepared to fight or possessed of a perfectly morbid curiosity would abandon a windward position. A wild and unreasonable hope filled Hornblower's breast; a ship of war at sea - thanks to England's maritime mastery - would be far more probably English than French. And this was the cruising ground of the Indefatigable, his own ship, stationed there specially to fulfil the double function of looking out for French commercedestroyers and intercepting French blockade-runners. A hundred miles from here she had put him and his prize crew on board the Marie Galante. It was a thousand to one, he exaggerated despairingly to himself, against any ship sighted being the Indefatigable. But - hope reasserted itself - the fact that she was coming down to investigate reduced the odds to ten to one at most. Less than ten to one.
He looked over at Neuville, trying to think his thoughts. The Pique was fast and handy, and there was a clear avenue of escape to leeward. The fact that the stranger had altered course towards them was a suspicious circumstance, but it was known that Indiamen, the richest prizes of all, had sometimes traded on the similarity of their appearance to that of ships of the line, and by showing a bold front had scared dangerous enemies away. That would be a temptation to a man eager to make a prize. At Neuville's orders all sail was set, ready for instant flight or pursuit, and, close-hauled, the Pique stood towards the stranger. It was not long before Hornblower, on the deck, caught a glimpse of a gleam of white, like a tiny grain of rice, far away on the horizon as the Pique lifted on a swell. Here came Matthews, red-faced and excited, running aft to Hornblower's side.
`That's the old Indefatigable, sir,' he said. `I swear it!' He sprang onto the rail, holding on by the shrouds, and stared under his hand.


My thoughts have gone increasingly the past few days to my son, Andrew, who died this year. I think this lovely poem reflects what I have been feeling.
That is a lovely way to celebrate the life of a loved one. I am so sorry for your loss.
This is a wonderful poem. Your son will always be with you and hold a special place in your heart, Bernadette.
A lovely piece to share. Thinking of you, B. Hugs.
It is indeed a lovely poem, and I'm pleased it gives you comfort after losing Andrew. Hope all is as well as possible with you and your family.
Bernadette, my heart goes out to you as you grapple with your big loss. If hugs helped I would send you a starship full.
Your poem is so beautiful and warmed me deep to the soul. This is how I always thought of this evening. Remembering, honouring and loving our ancestors and loved ones that gone before.
So with you and many around the globe that is what I will do.
There is no greater loss than that of losing a child. You have had a lot to grapple with this year. The poem is beautiful. Andrew lives forever in your heart.
Beautiful poem, Bernadette. Andrew will always be in your heart. Sending hugs.
My heart still aches for your loss Bernadette. May God bless you and give you comfort during your time of loving and longing.. ❤ A beautiful poem..


Robert and Paulette Oleson are a recently married couple who've turned business partners and will use their background to successfully take over The Cleaning Authority of Kenosha this May.
Newlywed couple turned business partners, Robert and Paulette Oleson are taking over operations of The Cleaning Authority in Kenosha, Wisconsin, this May. The two have shared experience in management and operations, most recently in the senior retirement community industry. When they decided to look into business ownership opportunities, they were reminded of the excellent experience they had as customers of The Cleaning Authority previously, and investigated the business offering of the company. They were thrilled to find that The Cleaning Authority provided a sophisticated model, infrastructure and opportunity to scale the business. The Olesons look forward to serving the Racine and Kenosha area communities while providing jobs, especially to women in need, through the business.
What were you doing before partnering with The Cleaning Authority?
We both worked in senior citizen community management, most recently in Albuquerque, New Mexico, before moving to Wisconsin. Previously, before we met, Robert had a career in corporate security and is also a Navy veteran. I worked for We Energies in Milwaukee, Wisconsin, before moving to the Southwest in 2015.
How did you learn about The Cleaning Authority, and what made you ultimately decide to commit?
We used The Cleaning Authority to clean our home when we lived in Wisconsin and knew the previous owner. When we were looking into owning our own business, we thought that the franchise system would fit our previous experiences and strengths and loved the service of The Cleaning Authority so much that we decided to buy the company ourselves. From a customer perspective, we know that the brand's services are better than competitors and as we learned about the business offering, it was clear that the company also has a strong model, infrastructure and support system.
We researched hundreds of franchise offerings and the main reason we selected The Cleaning Authority was the corporate support. Everything from the marketing to IT support and corporate call center really seems to set franchisees up for success. The support provided by the corporate team combined with an autonomy to run our business and control our success exceeded our expectations.
If you were to speak with someone who's considering signing on with The Cleaning Authority, what advice would you give them?
It is important to recognize that while the corporate office will support your success, they cannot do everything for you to make your individual business successful. You need to be prepared to put in a lot of work to get the business up and running and maintain a steady base of customers.
When I worked at We Energies in Milwaukee previously, I was the president of the Women's Development Network. I hope to incorporate my previous leadership in that area in order to reach out and provide opportunities to women in the area who are in need of jobs.


n. 1. A young man living as an apprentice on a sheep station, or otherwise engaged in acquainting himself with colonial life.
v. i. 1. To be a jackaroo; to pass one's time as a jackaroo.
Besides the eccentric central characters, the script featured oddball minor roles such as the dancing jackaroos on the ranch where Flo takes refuge from her family.
The green and orange hues of the ranch's interiors, where laid-back jackaroos share the domestic tasks, echo the harmonious tones of the exterior landscape.
Similarly, the much-discussed episode showing two jackaroos dancing together before the party could be part of the narrative, as they practice their steps for the upcoming dance, or a shot of the actors rehearsing on the set before shooting the dance scene.
It s shaping up to be a stellar tournament with the Australian Jackaroos and New Zealand Black Jacks ready to battle it out, fresh from recently competing at the Eight Nation Commonwealth Games invitational event in Scotland.
Local employment opportunities were limited, particularly for girls, and traditional rural jobs such as jackaroos and jillaroos (male and female station hands respectively) were scarce.
My job was cooking on the homestead but I was also lucky enough to go out on stock camp a couple of times with one of the inspectors to stay with the Jills and Jackaroos - the cowgirls and cowboys.
Many jackaroos and stockmen on the country's huge cattle ranches, or stations, have grown accustomed since the 1960s to rounding up herds with helicopters, motorbikes, and four-wheel drives.
In Australia, cowboys are called jackaroos but being in charge of the enormous cattle stations in the Northern Territory isn't just a job for the boys.
After a huge cooked breakfast made by Allana the cook, jackaroos Kurt Steiger, 24, Shaun Davey, 19, and his cousin Warren Green, 19, are saddling up their horses.
He eventually left the sheep station to become a cameraman at the ABC in Sydney, later returning to the farm to film a documentary about jackaroos.
As time went on, I knew I didn't want to be a jackaroo forever; but I looked at the little camera that had been recording this world I enjoyed so much, and the thought dawned--wouldn't it be great to go round the world recording places and people and things that other people might never get to see themselves, but could experience through film.


Ocean Oddities is a video slot available at All Star Slots that uses a format with five reels, three rows and 25 paylines. It has a really fun deep sea theme with a lot of fish that behave in atypical ways. This includes barking sharks, snails riding seahorses and all kinds of crazy action. What's more is that this game has a medium volatility, so you get the perfect mix of chances for big jackpots and plenty of small and medium prizes. Overall, it's an atypical game with an atypical theme and great payouts.
Wild Symbol - The wild Rex symbol shows up on the last four reels, so there is no payout for five of a kind in wilds.
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Free Spins Bonus Round - Three or more of the scattered Pearl symbol gives players a set of 10 free spins.
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Explore the depths of the ocean and win big by discovering the jackpot of treasure when your download our free software today.
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Photos / Sanjana Kapoor Photogallery
Sanjana Kapoor Photos
Last updated on May 16, 2020, 20.44
Kapoor Family
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Q: rsync: Get diff output of file and something similar as a merge Use-Case
I use rsync to sync my files between two machines. Assuming I want to sync /important/file.txt from machine A to B, I did some changes on machine A t /important/file.txt and somenone else added some changes to /important/file.txt as well. So I'd do the following first before the actual sync to avoid accidental removings:
rsync -aun -Ph machineB:/important/file.txt /important/file.txt

and now I get the following output:
/important/file.txt

obviously it tells me that it wants to overwrite my /important/file.txt but I'd like to do a merge as I'd do git mergetool.
Questions

*

*What's the best way to get a neat diff of the local and remote /important/file.txt? I thought about to quickly fetch the file to a random place like:
rsync machineB:/important/file.txt /tmp/file.txt

and then do a diff -y /important/file.txt /tmp/file.txt but maybe there's a better way?

*What would you recommend to have a similar behaviour as with git mergetool? Because in my example above I've a "merge conflict" since I on machine A and the person on machine B did some changes to /important/file.txt, now a merging behaviour where you can see the local changes with the remote changes would be neat in my opinion. I'm aware that I might have to use something else than rsync for this since rsync doesn't know the "base version" of the file. What would you recommend here?

redpajama_set_name: RedPajamaStackExchange


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Q: Output pre-json encoded string to spring framework I have a json:object I'm serving.  As part of that json document, I want to serve some pre-encoded json.  unfortunately, once served, the pre-encoded json is re-encoded.  Is there a way to escape that property so it's simply served?
<json:property name="data"><c:out value="${overlay.boundry}"/></json:property>

A: I assume you mean that overlay.boundry been HTML encoded. If so, then you just need to remove the c:out tag like this:
<json:property name="data">${overlay.boundry}</json:property>

or, if you really like JSTL tags:
<json:property name="data"><c:out value="${overlay.boundry}" escapeXml="false" /></json:property>


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Q: Find all finite dimensional simple Lie algebras satisfying certain conditions Let $\mathfrak{g}$ be a finite dimensional simple Lie algebra over $\mathbb{C}$. Suppose that $\mathfrak{g}$ can be generated by five nonzero elements $x,y,x',y',h\in \mathfrak{g}$, which satisfy the following relations:
$$[x,y]=h, [h,x]=2x, [h,y]=-2y\tag{1}$$
$$[x',y']=h, [h,x']=2x', [h,y']=-2y'\tag{2}$$
$$[x,x']=[y,y']=0\tag{3}$$
Basically, $\{x,y,h\}$ and $\{x',y',h\}$ each form a $\mathfrak{sl}(2)$, sharing the same CSA, and with $[x,x']=[y,y']=0$. We can represent the relations graphically as follows:

Question: what are all possibilities of $\mathfrak{g}$? My conjecture is that $\mathfrak{g}$ can only be $\mathfrak{sl}(2)$, with $x=\lambda x', y'=\lambda y$, for some $\lambda\in \mathbb{C}$, but I have no idea how to prove it.
[A vague idea: maybe we can first prove that there exist $f\in \mathrm{Aut}(\mathfrak{g})$ with $f(x)=x',f(y)=y',f(h)=h$, and then use our knowledge of automorphisms of simple Lie algebra to restrict the possibilities of $\mathfrak{g}$?]

A: EDIT: [Failed argument follows in the first paragraph, left here for posterity.] I think this is quite straightforward - in any finite-dimensional quotient ${\mathfrak s}$ of your Lie algebra, $h$ is semisimple (since it acts via scalar multiplication of each generator) and $x,y,x',y'$ are nilpotent (since they are eigenvectors for $h$, with non-zero eigenvalues). Now all eigenvalues of $({\rm ad}\, h)$ on ${\mathfrak s}$ are real (since this is true for the generators) so there exists a Cartan subalgebra ${\mathfrak h}$ containing $h$, and (assuming ${\mathfrak s}$ is simple) a positive system $\Phi^+$ in $\Phi({\mathfrak s},{\mathfrak h})$ such that all weights of $h$ on $\Phi^+$ are non-negative. In particular, this means $x,x'$ are sums of positive root vectors and $y,y'$ are sums of negative root vectors. It follows immediately that $h$ spans ${\mathfrak h}$ [this doesn't actually follow], so ${\mathfrak s}$ is of rank 1, so equals $\mathfrak{sl}_2$. Hence $x$ and $x'$ both map to some (non-zero) multiple of $e$, and we get your ideals $x-\lambda x'$, $y'-\lambda y$. (You need $\lambda\neq 0$.)
I couldn't help making an observation. A more natural presentation of your Lie algebra is:
$$[e_1,f_1]=h_1,\;\; [h_1,e_1]=2e_1,\;\; [h_1,f_1]=2f_1,$$
$$[e_2,f_2]=h_2,\;\; [h_2,e_2]=2e_2, \;\; [h_2,f_2]=-2f_2,$$
$$[e_1,f_2]=[e_2,f_1]=0,\;\; h_1+h_2=0$$
where $e_1=x$, $f_1=y$, $e_2=y'$, $f_2=x'$.
In other words, $x$ and $y'$ are the positive root elements, and $x'$ and $y$ are the negative root elements (different from the above). This is certainly an infinite-dimensional Lie algebra. If we quotient further by the conditions $$({\rm ad}\, e_1)^3(e_2)=({\rm ad}\, e_2)^3(e_1)=0$$ and similarly for $f_1, f_2$ then we obtain the loop algebra $\mathfrak{sl}_2\otimes{\mathbb C}[t,t^{-1}]$. (This follows from the Gabber-Kac theorem - these relations without the condition $h_1+h_2=0$ generate the derived subalgebra of the affine Kac-Moody algebra of type $A_1$; then $h_1+h_2$ is in the centre, and taking the quotient by it produces the loop algebra. Going in reverse, one would construct the affine $A_1$ Lie algebra as a central extension of $\mathfrak{sl}_2\otimes{\mathbb C}[t,t^{-1}]$.)
The map from your Lie algebra to $\mathfrak{sl}_2\otimes{\mathbb C}[t,t^{-1}]$ is given by: $$x\mapsto e\otimes 1,\; y\mapsto f\otimes 1,\; h\mapsto h\otimes 1,\; y'\mapsto f\otimes t,\; x'\mapsto e\otimes t^{-1}.$$
FURTHER EDIT: Ok, the loop algebra does actually help. If ${\mathfrak s}$ is a finite-dimensional simple quotient of your Lie algebra, then the images of $x,y,h$ span an $\mathfrak{sl}_2$-triple, and $x'$ is in the 2-weight space for $h$, and we have $[x,x']=0$, so $x'$ is a highest weight vector for the $\mathfrak{sl}_2$. It follows that $({\rm ad}\, y)^3(x')=0$. Exactly the same argument establishes $({\rm ad}\, y')^3(x)=0$ etc. so in fact any finite-dimensional quotient of your Lie algebra factors through the surjection onto the loop algebra. I think the only finite-dimensional simple quotient of the loop algebra is $\mathfrak{sl}_2$.


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