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Pipeline Technology
Much has changed in the design and operations of oil pipelines since the first were built in Canada and the United States during the 1860s. Those early small-diameter pipelines have long since been decommissioned, and modern-day pipelines benefit from some of the most advanced and environmentally-conscious technology available:
Centralized Control Centre
Centralized Control Centre monitors flow rates, pressures and fluid characteristics 24 hours a day, seven days a week. Fluctuations can be quickly detected, alerting operators to potential leaks, and allowing them to shutdown lines and dispatch crews.
Check valves can only open when upstream pressure exceeds downstream pressure. If the downstream pressure exceeds upstream pressure for any reason, then the valve automatically closes and reverse flow in the pipeline is blocked.
Block Valves are typically automated and can be controlled remotely. They feature an electric actuator that is connected via satellite or other communications system. If a problem is detected and sent to the Control Centre as an alarm, the operator will follow written procedures, which may include stopping the pipeline and closing the Block Valves to isolate the area until the condition can be investigated and resolved.
High-Performance Coating
High-performance coating systems greatly reduce corrosion hazards.
Smart Pigs
Internal inspection tools called Smart Pigs are sent down the pipeline with the product. Carrying onboard computers and sensors, they measure the diameter of the pipe and the thickness of the pipe wall and can detect dents, gouges or other damage to pipeline. Ultrasonic or EMAT (Electro magnetic acoustical transmission) testing further detects signs of any corrosion or cracks that have initiated in the pipe.


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Tags: rock music
Piano 3
This issue is dedicated to Nordic music. It features interviews with award-winning Finnish film composer Tuomas Kantelinen, Icelandic band Sykur and…Standard / 8.25" x 10.75"Print + Digital: $12.00 Digital: $2.99
The Wedding Dress
This is about 'The Wedding Dress' - a Rock music concept album for the women's market. By Fran May, with Richard Newman on guitar.Standard / 8.25" x 10.75"Print + Digital: $20.00 Digital: Free!
Kickstart Unsigned e-mag
Online magazine for unsigned artistsSquare / 8" x 8"Print: $5.50 Digital: $3.50
Northwest Alternative: Northwest Alternative #2
Issue 2 : Features in depth interviews with burlesque dancer Sydni Deveraux & pin striper El Volo, the amazing artwork of Rebecca Cliborne (Kotsu),…Digest / 5.25" x 8.25"Print + Digital: $8.50 Digital: $3.50
Greek Fire: Just the Beginning
A collection of photos of the rock band Greek Fire. 9 shows during 2011, including St. Louis, MO., Chicago, IL. and Milwaukee, WI. Photographed by…Digest / 8.25" x 5.25"Print + Digital: $15.95 Digital: $5.00

subset: commoncrawl


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News & Announcements
Incoming Brody students don white coatsThird-year medical student Caitlin Durr was wearing a white coat in 90-degree heat at noon Aug. 5, but she still had goosebumps. She was preparing to lead her newest classmates in a pledge of ethics as part of the 17th white coat ceremony at the Brody School of Medicine.
Brody receives award for social accountability
The way East Carolina University's medical students serve the communities of North Carolina is earning international recognition for the Brody School of Medicine. Brody is one of seven schools globally to receive a 2016 Aspire to Excellence Award, which recognizes excellence in education at medical, dental and veterinary schools.
ECU telepsychiatry reaches patients across NCThe North Carolina Statewide Telepsychiatry Program offers unprecedented access through an innovative delivery system connecting qualified doctors to mental health and substance abuse patients who sorely need their help. It is altering the landscape of psychiatric treatment and availability in the state.
Carabello, Kiser join ECU Physicians cardiology
The Brody School of Medicine at East Carolina University and Vidant Medical Center have appointed two acclaimed specialists to key leadership positions. Drs. Blase Carabello and Andy Kiser bring international experience and a new level of expertise in cardiovascular care to the East.
Learn about the BSOM threefold mission and the steps we're taking to both preserve this mission and build our future.
We're seeking an energetic, experienced, visionary leader who values collaboration, diversity and service.
REACH (Redesigning Education to Accelerate Change in Healthcare) is transforming the BSOM curriculum.
Quick Links
Upcoming Events
Stay Connected


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My Previous Post > "GM Our Town, Our Heroes: Escalade Hybrid the Lap of Luxury"
I nearly fell off the couch when I read the email:
Chevrolet Invites You to a Chicago Cubs Game
To thank you for being a Hero, we would also like to honor your good work by recognizing you on the field…
What? Who, me? Are you serious?!?
I thought the week long use of the Cadillac Escalade Hybrid, the $100 gift card and the trunk full of toys for the kids battling childhood cancer at The University of Chicago Comer Children's Hospital was the extent of my reward for being selected a GM Hero. It was more than enough.
But there it was, I had been invited by GM (Chevrolet) to the August 22nd Chicago Cubs game to be recognized on the field – WRIGLEY FIELD!
Okay. Okay. So my friends and family will be the first to tell you that I'm not exactly a sports fan. I mean, I like sports – in high school I was on pom-poms so I attended all the football and basketball games. In college, for my 20th birthday I received courtside tickets to a Chicago Bulls game when Jordan, Pippen and Rodman were the trifecta – but now, these days, I don't watch many sports and I really have little allegiance to any team.
However, and this is a big however, I have Chicago Cubs blood coursing through my veins, so my non-sports-lovin' self was on Cloud 9 to learn of such an incredible opportunity.
You see…
My grandpa worked at WGN-TV for forty years before retiring. He was an engineer/camera man, filming live commercials, local children's shows (like Bozo's Circus and Garfield Goose) and the Chicago Cubs games at Wrigley Field. Growing up I'd heard – about a million times! – how as kids my mom, aunts and uncles used to sit in the coveted seats behind the dugout while grandpa was working. I'm not sure that's a benefit cameramen get these days.
My grandpa retired from WGN many years ago, and it had been 23 years since he'd been back to Wrigley Field.
I was invited to bring a guest, so after thinking about it I decided to bring my husband, Steve (just joking – he is always my first choice). Of course, my mom was the second person I told and immediately she started working on securing tickets for herself. I was thrilled to know she wanted to be there. She ended up getting two tickets – one for her and one for my grandpa!
Upon arriving at Wrigley Field, we met our Chevrolet host, Mark Jenkins, our MSL Chicago host, Dawn McKenzie and Donald Pannier, selected as a Hero for his dedication and service to the Illinois Patriot Guard Fallen Heroes Traveling Memorial Wall in memory of his son.
We were escorted to seats near the field. Shortly thereafter, we were called onto the field to be formally introduced as GM Heroes. From the few games that I'd actually attended, I'd always wondered who those people were, that were being announced and specifically what they'd done to receive such an honor, and there I was.
I was one of "those people." It was incredible hearing my name booming across the stadium. Proudly, I stood next to Steve. I was beaming; he was beaming; my mom and grandpa were beaming. It was a beautiful, special moment!
Afterward, we went to our seats and were treated with hot dogs, beer and anything else we wanted. The game was fun. We took lots of pictures. I cherished everything about it, especially sitting next to Steve, mom and grandpa. I knew it would probably never happen again.
Unfortunately, the Cubs lost, but who cared?!? Nothing could squash our spirits… Surprisingly, I got into the game and actually yelled out "That's bullsh*t!" in response to the last play of the night when the empire called us out. Not very Hero-ish; I don't know what came over me. I guess it's that Chicago Cubs blood coursing through my veins!
I'll always be a fan, no matter what.
Being there with my grandpa, sharing this moment with my mom and standing beside my husband on the field was an experience I will never forget.
I'm so glad that my grandpa got a chance to visit his old stomping grounds and be immersed in the wonderful memories of days gone by. I'm so proud that he saw his granddaughter recognized in the very place he'd worked so long ago.
During the game, my mom leaned over to me and whispered, "All those years ago, I never would have imagined MY daughter standing on the field for all to see, being recognized for her good work."
It made my heart sing!
Thank you GM for the many, many gifts – even the ones you could have never known you were giving me.
Next >"Childhood Vacation Memories"
Filed under: Uncategorized
Tags: Atia's Project Ladybug fund, Baseball, Cancer, Chicago Cubs, childhood cancer, Comer Children's Hospital. U of C, Dawn McKenzie, Donald Pannier, General Motors, Hero Award, Illinois Patriot Guard Fallen Heroes Traveling Memorial Wall, Mark Jenkins, MSL Chicago, Our Town Our Heroes, pediatric cancer, Project Ladybug, The University of Chicago Comer Children's Hospital, WGN, WGN-TV, Wrigley Field


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Book your room at Fairfield Harbour Guest Rooms
Get an overview of this hotelRiverfront hotel with golf course and restaurant
Situated on the waterfront, this hotel is 0.1 mi (0.1 km) from Northwest Creek Marina and within 12 mi (20 km) of Pepsi Museum and New Bern Firemen's Museum. Tryon Palace is 13 mi (20.9 km) away.
Hotel Features
A golf course, a restaurant, and an indoor pool are available at this hotel. Free WiFi in public areas and free self parking are also provided. Additionally, a fitness center, a bar/lounge, and outdoor tennis courts are onsite.
Room Amenities
All 5 individually furnished rooms feature free WiFi and room service. Comforts include premium bedding and down comforters, and guests will also find conveniences like refrigerators and microwaves.Would you like to give us feedback? Share it! Opens in a new window
Fairfield Harbour Guest Rooms100 Marina Drive New Bern NC 28560
Hotel Amenities
Hotel Amenities
In addition to a golf course, Fairfield Harbour Guest Rooms features outdoor tennis courts and an indoor pool. The hotel offers a restaurant. A bar/lounge is on site where guests can unwind with a drink. High-speed wireless Internet access is complimentary.
This New Bern hotel also offers a seasonal outdoor pool, a spa tub, and a fitness center. Guests can use the indoor pool, outdoor pool, and health club at a partner hotel. Complimentary self parking is available on site.
- Outdoor tennis courts - 2
- Pool umbrellas
- Outdoor seasonal pool
- Fitness facilities
- Pool sun loungers
- Total number of rooms - 5
- Number of floors - 2
- Tours/ticket assistance
- Golf course on site
- Free self parking
- Number of buildings/towers - 1
- Bar/lounge
- Free WiFi
- Restaurant
- Sauna
- Spa tub
- Indoor pool
Family Friendly Amenities
- Family Hotel
- Indoor pool
- Free Wi-Fi
- Outdoor tennis courts
- Playground on site
- Miniature golf on site
- Refrigerator
- Microwave
Available in all rooms: Free WiFi
Available in some public areas: Free WiFi
Free self parking
Room Amenities
- Air conditioning
- Free toiletries
- Hair dryer (on request)
- Iron/ironing board (on request)
- Premium bedding
- Refrigerator
- Coffee/tea maker
- Microwave
- Private bathroom
- Shower only
- Room service (limited hours)
- Individually furnished
- Cable TV service
- Free WiFi
- Down comforter
Where to Eat
Fairfield Harbour Dining - This restaurant specializes in seafood and serves breakfast, lunch, and dinner. Guests can order drinks at the bar and enjoy alfresco dining (weather permitting).
Room service (during limited hours) is available.
Nearby Things to Do
Guests can play rounds at the 18-hole golf course and enjoy other recreation facilities including outdoor tennis courts. An indoor pool, a seasonal outdoor pool, and a spa tub are on site. Other recreational amenities include a sauna and a fitness center.
The recreational activities listed below are available either on site or nearby; fees may apply.
- Bicycle rentals nearby
- Golfing nearby
- Kayaking nearby
- Sailing nearby
- Hiking/biking trails nearby
- Fishing on site
- Miniature golf on site
- Playground on site
- Boat tours nearby
To make requests for specific accessibility needs, complete the "Special or Accessibility Requests" section of "Trip Preferences" when you book your hotel.
Hotel Policies
Check-in time starts at 3 PM
Check-in time ends at 5 PM
Minimum check-in age is 21
Special check-in instructions:
Check-out time is 11 AM
Payment types
- Pets not allowed (service dogs only)
You need to know
Extra-person charges may apply and vary depending on hotel policy.
Government-issued photo identification and a credit card or cash deposit are required at check-in for incidental charges.
Special requests are subject to availability upon check-in and may incur additional charges. Special requests cannot be guaranteed.
- The name on the credit card used at check-in to pay for incidentals must be the primary name on the guestroom reservation.
Only service animals are allowed
No rollaway/extra beds available
No cribs (infant beds) available
No elevators
Optional extras
- Facilities fee: USD 5 per person, per day and includes use of:
Hotel Name
- Hurricane Resort-Restaurant Guest Rooms Hotel
- Hurricane Resort-Restaurant Guest Rooms Hotel New Bern
- Hurricane Resort-Restaurant Guest Rooms New Bern
- Fairfield Harbour Guest Rooms Hotel New Bern
- Fairfield Harbour Guest Rooms Hotel
- Fairfield Harbour Guest Rooms New Bern
- Fairfield Harbour Guest Rooms
- The Hurricane Resort Restaurant Guest Rooms
We should mention
One child 9 years old or younger stays free when occupying the parent or guardian's room, using existing bedding. Only registered guests are allowed in the guestrooms. Some facilities may have restricted access. Guests can contact the property for details using the contact information on the booking confirmation.


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Announced this morning, OnePlus is partnering up with SwiftKey, the makers of the highly popular third party keyboard, bringing the app preinstalled on the next round of OTA updates to One owners.
With the integration of the SwiftKey keyboard app right into CyanogenMod 11S, users will no longer need to head into Google Play to download it, and can simply turn it on from the Settings menu. (more…)


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Most Cited Brain Research Articles
The most cited articles published since 2011, extracted from Scopus.
Etiological heterogeneity in autism spectrum disorders: More than 100 genetic and genomic disorders and still countingCatalina Betancur
Volume 1380, Issue , March 2011, Pages 42-77
There is increasing evidence that autism spectrum disorders (ASDs) can arise from rare highly penetrant mutations and genomic imbalances. The rare nature of these variants, and the often differing orbits of clinical and research geneticists, can make it difficult to fully appreciate the extent to which we have made progress in understanding the genetic etiology of autism. In fact, there is a persistent view in the autism research community that there are only a modest number of autism loci known. We carried out an exhaustive review of the clinical genetics and research genetics literature in an attempt to collate all genes and recurrent genomic imbalances that have been implicated in the etiology of ASD. We provide data on 103 disease genes and 44 genomic loci reported in subjects with ASD or autistic behavior. These genes and loci have all been causally implicated in intellectual disability, indicating that these two neurodevelopmental disorders share common genetic bases. A genetic overlap between ASD and epilepsy is also apparent in many cases. Taken together, these findings clearly show that autism is not a single clinical entity but a behavioral manifestation of tens or perhaps hundreds of genetic and genomic disorders. Increased recognition of the etiological heterogeneity of ASD will greatly expand the number of target genes for neurobiological investigations and thereby provide additional avenues for the development of pathway-based pharmacotherapy. Finally, the data provide strong support for high-resolution DNA microarrays as well as whole-exome and whole-genome sequencing as critical approaches for identifying the genetic causes of ASDs. © 2010 Elsevier B.V. All rights reserved.
Brain growth across the life span in autism: Age-specific changes in anatomical pathologyEric Courchesne | Kathleen Campbell | Stephanie Solso
Volume 1380, Issue , March 2011, Pages 138-145
Autism is marked by overgrowth of the brain at the earliest ages but not at older ages when decreases in structural volumes and neuron numbers are observed instead. This has led to the theory of age-specific anatomic abnormalities in autism. Here we report age-related changes in brain size in autistic and typical subjects from 12 months to 50 years of age based on analyses of 586 longitudinal and cross-sectional MRI scans. This dataset is several times larger than the largest autism study to date. Results demonstrate early brain overgrowth during infancy and the toddler years in autistic boys and girls, followed by an accelerated rate of decline in size and perhaps degeneration from adolescence to late middle age in this disorder. We theorize that underlying these age-specific changes in anatomic abnormalities in autism, there may also be age-specific changes in gene expression, molecular, synaptic, cellular, and circuit abnormalities. A peak age for detecting and studying the earliest fundamental biological underpinnings of autism is prenatal life and the first three postnatal years. Studies of the older autistic brain may not address original causes but are essential to discovering how best to help the older aging autistic person. Lastly, the theory of age-specific anatomic abnormalities in autism has broad implications for a wide range of work on the disorder including the design, validation, and interpretation of animal model, lymphocyte gene expression, brain gene expression, and genotype/CNV-anatomic phenotype studies. © 2010 Elsevier B.V. All rights reserved.
The tip of the iceberg: RNA-binding proteins with prion-like domains in neurodegenerative diseaseOliver D. King | Aaron D. Gitler | James Shorter
Volume 1462, Issue , June 2012, Pages 61-80
Prions are self-templating protein conformers that are naturally transmitted between individuals and promote phenotypic change. In yeast, prion-encoded phenotypes can be beneficial, neutral or deleterious depending upon genetic background and environmental conditions. A distinctive and portable 'prion domain' enriched in asparagine, glutamine, tyrosine and glycine residues unifies the majority of yeast prion proteins. Deletion of this domain precludes prionogenesis and appending this domain to reporter proteins can confer prionogenicity. An algorithm designed to detect prion domains has successfully identified 19 domains that can confer prion behavior. Scouring the human genome with this algorithm enriches a select group of RNA-binding proteins harboring a canonical RNA recognition motif (RRM) and a putative prion domain. Indeed, of 210 human RRM-bearing proteins, 29 have a putative prion domain, and 12 of these are in the top 60 prion candidates in the entire genome. Startlingly, these RNA-binding prion candidates are inexorably emerging, one by one, in the pathology and genetics of devastating neurodegenerative disorders, including: amyotrophic lateral sclerosis (ALS), frontotemporal lobar degeneration with ubiquitin-positive inclusions (FTLD-U), Alzheimer's disease and Huntington's disease. For example, FUS and TDP-43, which rank 1st and 10th among RRM-bearing prion candidates, form cytoplasmic inclusions in the degenerating motor neurons of ALS patients and mutations in TDP-43 and FUS cause familial ALS. Recently, perturbed RNA-binding proteostasis of TAF15, which is the 2nd ranked RRM-bearing prion candidate, has been connected with ALS and FTLD-U. We strongly suspect that we have now merely reached the tip of the iceberg. We predict that additional RNA-binding prion candidates identified by our algorithm will soon surface as genetic modifiers or causes of diverse neurodegenerative conditions. Indeed, simple prion-like transfer mechanisms involving the prion domains of RNA-binding proteins could underlie the classical non-cell-autonomous emanation of neurodegenerative pathology from originating epicenters to neighboring portions of the nervous system. This article is part of a Special Issue entitled RNA-Binding Proteins. © 2012 Elsevier B.V.
The effects of acute exercise on cognitive performance: A meta-analysisY. K. Chang | J. D. Labban | J. I. Gapin | J. L. Etnier
Volume 1453, Issue , May 2012, Pages 87-101
There is a substantial body of literature related to the effects of a single session of exercise on cognitive performance. The premise underlying this research is that physiological changes in response to exercise have implications for cognitive function. This literature has been reviewed both narratively and meta-analytically and, although the research findings are mixed, researchers have generally concluded that there is a small positive effect. The purpose of this meta-analysis was to provide an updated comprehensive analysis of the extant literature on acute exercise and cognitive performance and to explore the effects of moderators that have implications for mechanisms of the effects. Searches of electronic databases and examinations of reference lists from relevant studies resulted in 79 studies meeting inclusion criteria. Consistent with past findings, analyses indicated that the overall effect was positive and small (g=0.097 n=1034). Positive and small effects were also found in all three acute exercise paradigms: during exercise (g=0.101; 95% confidence interval CI]; 0.041-0.160), immediately following exercise (g=0.108; 95% CI; 0.069-0.147), and after a delay (g=0.103; 95% CI; 0.035-0.170). Examination of potential moderators indicated that exercise duration, exercise intensity, type of cognitive performance assessed, and participant fitness were significant moderators. In conclusion, the effects of acute exercise on cognitive performance are generally small; however, larger effects are possible for particular cognitive outcomes and when specific exercise parameters are used. © 2012 Elsevier B.V. All rights reserved.
Oophorectomy, menopause, estrogen treatment, and cognitive aging: Clinical evidence for a window of opportunityWalter A. Rocca | Brandon R. Grossardt | Lynne T. Shuster
Volume 1379, Issue , March 2011, Pages 188-198
The neuroprotective effects of estrogen have been demonstrated consistently in cellular and animal studies but the evidence in women remains conflicted. We explored the window of opportunity hypothesis in relation to cognitive aging and dementia. In particular, we reviewed existing literature, reanalyzed some of our data, and combined results graphically. Current evidence suggests that estrogen may have beneficial, neutral, or detrimental effects on the brain depending on age at the time of treatment, type of menopause (natural versus medically or surgically induced), or stage of menopause. The comparison of women who underwent bilateral oophorectomy with referent women provided evidence for a sizeable neuroprotective effect of estrogen before age 50 years. Several case-control studies and cohort studies also showed neuroprotective effects in women who received estrogen treatment (ET) in the early postmenopausal stage (most commonly at ages 50-60 years). The majority of women in those observational studies had undergone natural menopause and were treated for the relief of menopausal symptoms. However, recent clinical trials by the Women's Health Initiative showed that women who initiated ET alone or in combination with a progestin in the late postmenopausal stage (ages 65-79 years) experienced an increased risk of dementia and cognitive decline regardless of the type of menopause. The current conflicting data can be explained by the window of opportunity hypothesis suggesting that the neuroprotective effects of estrogen depend on age at the time of administration, type of menopause, and stage of menopause. Therefore, women who underwent bilateral oophorectomy before the onset of menopause or women who experienced premature or early natural menopause should be considered for hormonal treatment until approximately age 51 years. © 2010 Elsevier B.V. All rights reserved.
Transplantation of human bone marrow-derived mesenchymal stem cells promotes behavioral recovery and endogenous neurogenesis after cerebral ischemia in ratsXinjie Bao | Junji Wei | Ming Feng | Shan Lu | Guilin Li | Wanchen Dou | Wenbin Ma | Sihai Ma | Yihua An | Chuan Qin | Robert Chunhua Zhao | Renzhi Wang
Volume 1367, Issue , January 2011, Pages 103-113
Mesenchymal stem cells (MSCs) have been successfully used for the treatment of experimental stroke. However, the neurorestorative mechanisms by which MSCs improve neurological functional recovery are not fully understood. Endogenous cell proliferation in the subventricular zone (SVZ) after stroke is well known, but most of newly formed cells underwent apoptosis. In the present study, we tested the hypothesis that neurotrophic factors secreted by human bone marrow-derived MSCs (hBMSCs) promote endogenous neurogenesis, reduce apoptosis, and improve functional recovery. Adult rats subjected to 2-h middle cerebral artery occlusion (MCAO) were transplanted with hBMSCs or saline into the ipsilateral brain parenchyma at 3 days after ischemia. There was a significant recovery of behavior in the hBMSCs-treated rats beginning at 14 days after MCAO compared with the control animals. Higher levels of brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and vascular endothelial growth factor (VEGF) were detected in the hBMSCs-treated rat brain than the control. Human BMSCs treatment also enhanced endogenous cell proliferation both in the SVZ and in the subgranular zone (SGZ) of the hippocampus. In addition, more neuronal progenitor cells migrated from the SVZ to the ischemic boundary zone (IBZ) and differentiated into mature neurons with less apoptosis in rats treated with hBMSCs. Overall, these data suggest an essential role for hBMSCs in promoting endogenous neurogenesis, protecting newly formed cells, and improving functional recovery after ischemia in rats. © 2010 Elsevier B.V. All rights reserved.
Sociability and motor functions in Shank1 mutant miceJill L. Silverman | Sarah M. Turner | Charlotte L. Barkan | Seda S. Tolu | Roheeni Saxena | Albert Y. Hung | Morgan Sheng | Jacqueline N. Crawley
Volume 1380, Issue , March 2011, Pages 120-137
Autism is a neurodevelopmental disorder characterized by aberrant reciprocal social interactions, impaired communication, and repetitive behaviors. While the etiology remains unclear, strong evidence exists for a genetic component, and several synaptic genes have been implicated. SHANK genes encode a family of synaptic scaffolding proteins located postsynaptically on excitatory synapses. Mutations in SHANK genes have been detected in several autistic individuals. To understand the consequences of SHANK mutations relevant to the diagnostic and associated symptoms of autism, comprehensive behavioral phenotyping on a line of Shank1 mutant mice was conducted on multiple measures of social interactions, social olfaction, repetitive behaviors, anxiety-related behaviors, motor functions, and a series of control measures for physical abilities. Results from our comprehensive behavioral phenotyping battery indicated that adult Shank1 null mutant mice were similar to their wildtype and heterozygous littermates on standardized measures of general health, neurological reflexes and sensory skills. Motor functions were reduced in the null mutants on open field activity, rotarod, and wire hang, replicating and extending previous findings (Hung et al., 2008). A partial anxiety-like phenotype was detected in the null mutants in some components of the light ↔ dark task, as previously reported (Hung et al., 2008) but not in the elevated plus-maze. Juvenile reciprocal social interactions did not differ across genotypes. Interpretation of adult social approach was confounded by a lack of normal sociability in wildtype and heterozygous littermates. All genotypes were able to discriminate social odors on an olfactory habituation/dishabituation task. All genotypes displayed relatively high levels of repetitive self-grooming. Our findings support the interpretation that Shank1 null mice do not demonstrate autism-relevant social interaction deficits, but confirm and extend a role for Shank1 in motor functions.
Breaking down the barrier: The effects of HIV-1 on the blood-brain barrierMarianne Strazza | Vanessa Pirrone | Brian Wigdahl | Michael R. Nonnemacher
Volume 1399, Issue , July 2011, Pages 96-115
Human immunodeficiency virus type 1 (HIV-1) primarily infects CD4 + T cells and cells of the monocyte-macrophage lineage, resulting in immunodeficiency in an infected patient. Along with this immune deficiency, HIV-1 has been linked to a number of neurological symptoms in the absence of opportunistic infections or other co-morbidities, suggesting that HIV-1 is able to cross the blood-brain barrier (BBB), enter the central nervous system (CNS), and cause neurocognitive impairment. HIV-1-infected monocyte-macrophages traverse the BBB and enter the CNS throughout the course of HIV-1 disease. Once in the brain, both free virus and virus-infected cells are able to infect neighboring resident microglia and astrocytes and possibly other cell types. HIV-1-infected cells in both the periphery and the CNS give rise to elevated levels of viral proteins, including gp120, Tat, and Nef, and of host inflammatory mediators such as cytokines and chemokines. It has been shown that the viral proteins may act alone or in concert with host cytokines and chemokines, affecting the integrity of the BBB. The pathological end point of these interactions may facilitate a positive feedback loop resulting in increased penetration of HIV into the CNS. It is proposed in this review that the dysregulation of the BBB during and after neuroinvasion is a critical component of the neuropathogenic process and that dysregulation of this protective barrier is caused by a combination of viral and host factors including secreted viral proteins, components of the inflammatory process, the aging process, therapeutics, and drug or alcohol abuse. © 2011 Elsevier B.V. All rights reserved.
MicroRNA-10b induces glioma cell invasion by modulating MMP-14 and uPAR expression via HOXD10Lihua Sun | Wei Yan | Yingyi Wang | Guan Sun | Hui Luo | Junxia Zhang | Xiefeng Wang | Yongping You | Zhengxiang Yang | Ning Liu
Volume 1389, Issue , May 2011, Pages 9-18
MicroRNAs are small endogenous noncoding RNAs, which modulate target gene expression by binding with target mRNA sequences in the 3′untranslated region (UTR) with an imperfect complementarity that inhibits the mRNA translation. Many microRNAs have been reported to function as tumor oncogenes or anti-oncogenes. Recently, more and more microRNAs have been reported to contribute to a tumor's invasive potential. Here, we show that microRNA-10b (miR-10b) was over-expressed in glioma samples and directly associated with the glioma's pathological grade and malignancy. We also found that miR-10b induced glioma cell invasion by modulating tumor invasion factors MMP-14 and uPAR expression via the direct target HOXD10. The miR-10b/HOXD10/MMP-14/uPAR signaling pathway might contribute to the invasion of glioma. Accordingly, glioma cells lost their invasive ability when treated with specific antisense oligonucleotides (miR-10b inhibitors), suggesting that miR-10b could be used as a new bio-target to cure glioma. © 2011 Elsevier B.V. All rights reserved.
Cooperation between the default mode network and the frontal-parietal network in the production of an internal train of thoughtJonathan Smallwood | Kevin Brown | Ben Baird | Jonathan W. Schooler
Volume 1428, Issue , January 2012, Pages 60-70
The ability to generate and sustain an internal train of thought unrelated to external reality frees an agent from the constraints of only acting on immediate, environmentally triggered events. The current paper proposes that such thought is produced through cooperation between autobiographical information provided by the default mode network and a frontal-parietal control network which helps sustain and buffer internal trains of thought against disruption by the external world. This hypothesis explains at least two features of the literature on internally guided thought. First, access to the top-down control system is a generally accepted prerequisite of conscious experience; this explains why activation of this system and default mode activity is often observed together during periods of internally guided thought. Second, because the top-down attentional control system has a limited capacity, internally and externally driven streams can come into conflict, with the result that perceptual information must be denied attentional amplification if the internal stream is to be maintained. This explains why internal thought is routinely associated with a state of perceptual decoupling, reflected in both measured anticorrelations between the default mode network and sensory areas and the manner in which task unrelated thoughts compromise task performance. This paper offers a hypothesis that should help to constrain and guide interpretations, investigations, and analyses of the neural processes involved in internally driven cognition. This article is part of a Special Issue entitled Special Issue The Cognitive Neuroscience. © 2011 Elsevier B.V. All rights reserved.
Getting real about Semantic Illusions: Rethinking the functional role of the P600 in language comprehensionHarm Brouwer | Hartmut Fitz | John Hoeks
Volume 1446, Issue , March 2012, Pages 127-143
In traditional theories of language comprehension, syntactic and semantic processing are inextricably linked. This assumption has been challenged by the 'Semantic Illusion Effect' found in studies using Event Related brain Potentials. Semantically anomalous sentences did not produce the expected increase in N400 amplitude but rather one in P600 amplitude. To explain these findings, complex models have been devised in which an independent semantic processing stream can arrive at a sentence interpretation that may differ from the interpretation prescribed by the syntactic structure of the sentence. We review five such multi-stream models and argue that they do not account for the full range of relevant results because they assume that the amplitude of the N400 indexes some form of semantic integration. Based on recent evidence we argue that N400 amplitude might reflect the retrieval of lexical information from memory. On this view, the absence of an N400-effect in Semantic Illusion sentences can be explained in terms of priming. Furthermore, we suggest that semantic integration, which has previously been linked to the N400 component, might be reflected in the P600 instead. When combined, these functional interpretations result in a single-stream account of language processing that can explain all of the Semantic Illusion data. © 2012 Elsevier B.V.
Altered white matter integrity in first-episode, treatment-naive young adults with major depressive disorder: A tract-based spatial statistics studyXueling Zhu | Xiang Wang | Jing Xiao | Mingtian Zhong | Jian Liao | Shuqiao Yao
Volume 1369, Issue , October 2011, Pages 223-229
Because most previous diffusion tensor imaging (DTI) studies have focused on late-life depression, this study examined the possible changes in brain white matter (WM) in first-episode, treatment-naive young adults with major depressive disorder (MDD). DTI was performed in 25 (10 males and 15 females) first-episode, treatment-naive young adult patients with MDD and 25 healthy controls matched for age, gender, and education. A whole-brain statistical comparison method called tract-based spatial statistics (TBSS) was used to analyze the data. Compared with healthy controls, patients with MDD showed decreased fractional anisotropy (FA) values in three WM tracts: the left anterior limb of the internal capsule, the right parahippocampal gyrus, and the left posterior cingulate cortex. Further analysis revealed that FA values in the left anterior limb of the internal capsule were negatively correlated with the severity of depressive symptoms. No regions showed higher FA in MDD patients than in controls. The present results support the hypothesis that altered WM integrity, especially in the cortical-subcortical neural circuit, may contribute to the pathophysiology of MDD. Furthermore, these findings provide novel evidence that microstructural abnormalities in WM may occur early in the course of depression. © 2010 Elsevier B.V. All rights reserved.
Structural and functional magnetic resonance imaging of autism spectrum disordersKimberly A. Stigler | Brenna C. McDonald | Amit Anand | Andrew J. Saykin | Christopher J. McDougle
Volume 1380, Issue , March 2011, Pages 146-161
The neurobiology of autism spectrum disorders (ASDs) has become increasingly understood since the advent of magnetic resonance imaging (MRI). Initial observations of an above-average head circumference were supported by structural MRI studies that found evidence of increased total brain volume and early rapid brain overgrowth in affected individuals. Subsequent research revealed consistent abnormalities in cortical gray and white matter volume in ASDs. The structural integrity and orientation of white matter have been further elucidated via diffusion tensor imaging methods. The emergence of functional MRI techniques led to an enhanced understanding of the neural circuitry of ASDs, demonstrating areas of dysfunctional cortical activation and atypical cortical specialization. These studies have provided evidence of underconnectivity in distributed cortical networks integral to the core impairments associated with ASDs. Abnormalities in the default-mode network during the resting state have also been identified. Overall, structural and functional MRI research has generated important insights into the neurobiology of ASDs. Additional research is needed to further delineate the underlying brain basis of this constellation of disorders. © 2010 Elsevier B.V. All rights reserved.
Is schizophrenia on the autism spectrum?Bryan H. King | Catherine Lord
Volume 1380, Issue , March 2011, Pages 34-41
With the ongoing consideration of the diagnostic criteria for mental disorders that is active in the Diagnostic and Statistical Manual of Mental Disorders (DSM-V) and International Classification of Diseases (ICD-11) revision processes, it is timely to review the phenomenological overlap between autism and schizophrenia. These disorders have at various times been regarded alternatively as closely related and as non-overlapping and incompatible. Nevertheless, there are several reports in the literature that have described individuals with both autism and schizophrenia, and the broader phenotypes of these disorders clearly intersect. Recent studies reveal theory of mind deficits in both disorders, and mirror neuron impairments also appear to be shared. There also may be similar connectivity deficits emerging in functional imaging studies, and both disorders share several genetic signals that are being identified through detection of copy number variants. Taken together, these data suggest that it may be time to revisit the possibility that these disorders are related. © 2010 Elsevier B.V. All rights reserved.
Ischemic postconditioning protects brain from ischemia/reperfusion injury by attenuating endoplasmic reticulum stress-induced apoptosis through PI3K-Akt pathwayYajing Yuan | Qulian Guo | Zhi Ye | Xia Pingping | Na Wang | Zongbin Song
Volume 1367, Issue , January 2011, Pages 85-93
Endoplasmic reticulum (ER) stress has been implicated in the pathology of cerebral ischemia. During prolonged period of stress or when the adaptive response fails, apoptotic cell death ensues. Cerebral ischemic postconditioning (Postcond) has been shown to reduce cerebral ischemia/reperfusion (I/R) injury in both focal and global cerebral ischemia model. However, the mechanism remains to be understood. This study aimed to elucidate whether Postcond attenuates brain I/R damage by suppressing ER stress-induced apoptosis and if the phosphatidylinositol-3kinase/Akt (PI3K/Akt) pathway is involved. A focal cerebral ischemia rat model was used in the study. Rat brain infarct size and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) positive cells in ischemic penumbra were assessed after reperfusion of the brain. The expressions of C/EBP-homologous protein (CHOP), caspase-12, glucose-regulated protein 78 (GRP78) and the phosphorylation of Akt (Ser473) in ischemic penumbra were measured after reperfusion. Our results showed that Postcond significantly attenuated brain I/R injury, as shown by reduction in infarct size, cell apoptosis, CHOP expression, caspase-12 activation and increase in GRP78 expression. LY294002, a phosphoinositide 3-kinase inhibitor, increased the number of TUNEL-positive cells suppressed by Postcond in penumbra. In addition, LY294002 diminished the effect of Postcond on the activation of CHOP, caspase-12 and GRP78. These results suggest that Postcond protects brain from I/R injury by suppressing ER stress-induced apoptosis and PI3K/Akt pathway is involved. © 2010 Elsevier B.V. All rights reserved.
Resveratrol improves neuron protection and functional recovery in rat model of spinal cord injuryChangjiang Liu | Zhibin Shi | Lihong Fan | Chen Zhang | Kunzheng Wang | Bo Wang
Volume 1374, Issue , February 2011, Pages 100-109
Researches on the pathology of spinal cord injury (SCI) have been recently focused on oxidative radicals stress and inflammation associated neuronal apoptosis. Resveratrol, a natural phenolic compound, has been extensively studied and shown a wide variety of health beneficial effects, including prevention of cardiovascular diseases and cancer and neuroprotective activities. However, the study of its potential role in neuroprotection and underlying mechanism in SCI model has been limited. In this study, we investigated the effect of resveratrol on neurologic functions and histopathologic changes after SCI and the mechanism underlying its neuroprotective effects. First, neuronal function after SCI was evaluated with Basso Beattle Bresnahan locomotor rating scale (BBB) and the result showed that injured animals treated with resveratrol showed a significant increase in BBB scores. Further, histopathological alternations were evaluated with HE and Nissl staining, showing a restored neural morphology and an increase of the number of neurons after resveratrol administration. To explore the underlying mechanism, anti-oxidation effect of resveratrol was assessed by measuring superoxide dismutase (SOD) activity and malondialdehyde (MDA) level after SCI. Resveratrol treatment reversed the decrease of SOD activity and increase of MDA level caused by SCI, suggesting its anti-oxidation role in response to the injury. In addition, resveratrol treatment suppressed immunoreactivity and expression of inflammatory cytokines including IL-1β, IL-10, TNF-α, and myeloperoxidase (MPO) after SCI, suggesting an anti-inflammation effect of resveratrol. Finally, resveratrol treatment inhibited injury-induced apoptosis as assessed by electrical microscopy and TUNEL staining and affected the expression level of apoptosis-related gene Bax, Bcl-2 and caspase-3, which indicated its anti-apoptosis role after SCI. Our data suggest that resveratrol significantly promotes the recovery of rat dorsal neuronal function after SCI, and this effect is related to its characteristics of anti-oxidation, anti-inflammation and anti-apoptosis. © 2011 Elsevier B.V. All rights reserved.
Abnormal tau, mitochondrial dysfunction, impaired axonal transport of mitochondria, and synaptic deprivation in Alzheimer's diseaseP. Hemachandra Reddy
Volume 1415, Issue , September 2011, Pages 136-148
Growing evidence suggests that amyloid beta (Aβ) and tau pathologies are strongly associated with mitochondrial dysfunction and neuronal damage in Alzheimer's disease (AD). Extensive research of AD postmortem brains, mouse and fly models, including triple transgenic AD mice and mutant tau mice, and cell culture studies revealed that tau hyperphosphorylation is caused by multiple factors, including intraneuronal Aβ-oligomers, chronic oxidative stress, reduced insulin-like growth factor 1, and astrocytic mediated-Aβ and caspase activation. Overexpressed and phosphorylated tau appears to impair axonal transport of organelles causing synapse starvation, depletion of ATP, and ultimately neuronal damage. This article evaluates the role of tau in mitochondrial dysfunction and assesses how hyperphosphorylated tau impairs axonal transport of organelles in AD neurons. © 2011 Elsevier B.V. All rights reserved.
Connexin and pannexin hemichannels in inflammatory responses of glia and neuronsMichael V L Bennett | Juan M. Garré | Juan A. Orellana | Felix F. Bukauskas | Maiken Nedergaard | Juan C. Sáez
Volume 1487, Issue , December 2012, Pages 3-15
Mammals express ∼20 different connexins, the main gap junction forming proteins in mammals, and 3 pannexins, homologs of innexins, the main gap junction forming proteins in invertebrates. In both classes of gap junction, each channel is formed by two hemichannels, one contributed by each of the coupled cells. There is now general, if not universal, agreement that hemichannels of both classes can open in response to various physiological and pathological stimuli when they are not apposed to another hemichannels and face the external milieu. Connexin (and likely pannexin) hemichannel permeability is consistent with that of the cell-cell channels and open hemichannels can be a release site for relatively large molecules such as ATP and glutamate, which can serve as transmitters between cells. Here we describe three experimental paradigms in which connexin and pannexin hemichannel signaling occurs. (1) In cultures of spinal astrocytes FGF-1 causes the release of ATP, and ATP causes opening of pannexin hemichannels, which then release further ATP. Subsequently, several hours later, connexin hemichannels are also opened by an unknown mechanism. Release of ATP appears to become self sustaining through action of P2X7 receptors to open pannexin hemichannels and then connexin hemichannels, both of which are ATP permeable. (2) Spinal cord injury by dropping a small weight on the exposed cord is followed by release of ATP in the region surrounding the primary lesion. This release is greatly reduced in a mouse in which Cx43 is knocked down in the astrocytes. Application of FGF-1 causes a similar release of ATP in the uninjured spinal cord, and an inhibitor of the FGF-1 receptor, PD173074, inhibits both FGF-1 and injury-induced release. Reduction in ATP release is associated with reduced inflammation and less secondary expansion of the lesion. (3) Cortical astrocytes in culture are permeabilized by hypoxia, and this effect is increased by high or zero glucose. The mechanism of permeabilization is opening of Cx43 hemichannels, which can lead to cell death. Activated microglia secrete TNF-α and IL-1β, which open connexin hemichannels in astrocytes. Astrocytes release ATP and glutamate which can kill neurons in co-culture through activation of neuronal pannexin hemichannels. These studies implicate two kinds of gap junction hemichannel in inflammatory responses and cell death. This article is part of a Special Issue entitled Electrical Synapses. © 2012 Elsevier B.V.
Gene and miRNA expression profiles in autism spectrum disordersMohammad M. Ghahramani Seno | Pingzhao Hu | Fuad G. Gwadry | Dalila Pinto | Christian R. Marshall | Guillermo Casallo | Stephen W. Scherer
Volume 1380, Issue , March 2011, Pages 85-97
Accumulating data indicate that there is significant genetic heterogeneity underlying the etiology in individuals diagnosed with autism spectrum disorder (ASD). Some rare and highly-penetrant gene variants and copy number variation (CNV) regions including NLGN3, NLGN4, NRXN1, SHANK2, SHANK3, PTCHD1, 1q21.1, maternally-inherited duplication of 15q11-q13, 16p11.2, amongst others, have been identified to be involved in ASD. Genome-wide association studies have identified other apparently low risk loci and in some other cases, ASD arises as a co-morbid phenotype with other medical genetic conditions (e.g. fragile X). The progress studying the genetics of ASD has largely been accomplished using genomic analyses of germline-derived DNA. Here, we used gene and miRNA expression profiling using cell-line derived total RNA to evaluate possible transcripts and networks of molecules involved in ASD. Our analysis identified several novel dysregulated genes and miRNAs in ASD compared with controls, including HEY1, SOX9, miR-486 and miR-181b. All of these are involved in nervous system development and function and some others, for example, are involved in NOTCH signaling networks (e.g. HEY1). Further, we found significant enrichment in molecules associated with neurological disorders such as Rett syndrome and those associated with nervous system development and function including long-term potentiation. Our data will provide a valuable resource for discovery purposes and for comparison to other gene expression-based, genome-wide DNA studies and other functional data. © 2010 Elsevier B.V. All rights reserved.
Cadherins and neuropsychiatric disordersChristoph Redies | Nicole Hertel | Christian A. Hübner
Volume 1470, Issue , August 2012, Pages 130-144
Cadherins mediate cell-cell adhesion but are also involved in intracellular signaling pathways associated with neuropsychiatric disease. Most of the ∼100 cadherins that are expressed in the brain exhibit characteristic spatiotemporal expression profiles. Cadherins have been shown to regulate neural tube regionalization, neuronal migration, gray matter differentiation, neural circuit formation, spine morphology, synapse formation and synaptic remodeling. The dysfunction of the cadherin-based adhesive system may alter functional connectivity and coherent information processing in the human brain in neuropsychiatric disease. Several neuropsychiatric disorders, such as epilepsy/mental retardation, autism, bipolar disease and schizophrenia, have been associated with cadherins, mostly by genome-wide association studies. For example, CDH15 and PCDH19 are associated with cognitive impairment; CDH5, CDH8, CDH9, CDH10, CDH13, CDH15, PCDH10, PCDH19 and PCDHb4 with autism; CDH7, CDH12, CDH18, PCDH12 and FAT with bipolar disease and schizophrenia; and CDH11, CDH12 and CDH13 with methamphetamine and alcohol dependency. To date, disease-causing mutations are established for PCDH19 in patients with epilepsy, cognitive impairment and/or autistic features. In conclusion, genes encoding members of the cadherin superfamily are of special interest in the pathogenesis of neuropsychiatric disease because cadherins play a pivotal role in the development of the neural circuitry as well as in mature synaptic function. © 2012 Elsevier B.V. Al l rights reserved.
Anti-TNF-α reduces amyloid plaques and tau phosphorylation and induces CD11c-positive dendritic-like cell in the APP/PS1 transgenic mouse brainsJian Quan Shi | Wei Shen | Jun Chen | Bian Rong Wang | Ling Ling Zhong | Yin Wei Zhu | Hai Qing Zhu | Qiao Quan Zhang | Ying Dong Zhang | Jun Xu
Volume 1368, Issue , January 2011, Pages 239-247
Inflammation plays an important role in the pathogenesis of Alzheimer's disease (AD). Overexpression of tumor necrosis factor-α (TNF-α) occurs in the AD brain. Recent clinical studies have shown that the anti-TNF-α therapy improves cognition function of AD patients rapidly. However, the underlying mechanism remains elusive. The present study investigates the effects of intracerebroventricular injection of the monoclonal TNF-α antibody, Infliximab, on the pathological features of AD in the APP/PS1 double transgenic mice. We found that Infliximab administration reduced the levels of TNF-α, amyloid plaques, and tau phosphorylation as early as three days after daily injection of 150 μg Infliximab for three days. The number of CD11c-positive dendritic-like cells and the expression of CD11c were found to be increased concurrently after Infliximab injection. These data suggested that the CD11c-positive dendritic-like cells might contribute to the Infliximab-induced reduction of AD-like pathology. Furthermore, our results support the use of anti-TNF-α for the treatment of AD. © 2010 Elsevier B.V. All rights reserved.
Neuroanatomical changes due to hearing loss and chronic tinnitus: A combined VBM and DTI studyFatima T. Husain | Roberto E. Medina | Caroline W. Davis | Yvonne Szymko-Bennett | Kristina Simonyan | Nathan M. Pajor | Barry Horwitz
Volume 1369, Issue , October 2011, Pages 74-88
Subjective tinnitus is the perception of sound in the absence of an external source. Tinnitus is often accompanied by hearing loss but not everyone with hearing loss experiences tinnitus. We examined neuroanatomical alterations associated with hearing loss and tinnitus in three groups of subjects: those with hearing loss with tinnitus, those with hearing loss without tinnitus and normal hearing controls without tinnitus. To examine changes in gray matter we used structural MRI scans and voxel-based morphometry (VBM) and to identify changes in white matter tract orientation we used diffusion tensor imaging (DTI). A major finding of our study was that there were both gray and white matter changes in the vicinity of the auditory cortex for subjects with hearing loss alone relative to those with tinnitus and those with normal hearing. We did not find significant changes in gray or white matter in subjects with tinnitus and hearing loss compared to normal hearing controls. VBM analysis revealed that individuals with hearing loss without tinnitus had gray matter decreases in anterior cingulate and superior and medial frontal gyri relative to those with hearing loss and tinnitus. Region-of-interest analysis revealed additional decreases in superior temporal gyrus for the hearing loss group compared to the tinnitus group. Investigating effects of hearing loss alone, we found gray matter decreases in superior and medial frontal gyri in participants with hearing loss compared to normal hearing controls. DTI analysis showed decreases in fractional anisotropy values in the right superior and inferior longitudinal fasciculi, corticospinal tract, inferior fronto-occipital tract, superior occipital fasciculus, and anterior thalamic radiation for the hearing loss group relative to normal hearing controls. In attempting to dissociate the effect of tinnitus from hearing loss, we observed that hearing loss rather than tinnitus had the greatest influence on gray and white matter alterations. © 2010 Elsevier B.V. All rights reserved.
IL-10 directly protects cortical neurons by activating PI-3 kinase and STAT-3 pathwaysSushil Sharma | Bing Yang | Xiaopei Xi | James C. Grotta | Jaroslaw Aronowski | Sean I. Savitz
Volume 1373, Issue , February 2011, Pages 189-194
IL-10 reduces pro-inflammatory responses after ischemic stroke primarily by acting on glia and endothelium, but relatively little is known about the direct effects of IL-10 on cortical neurons, which are often damaged in stroke. We found by PCR and immunohistochemistry that cortical neurons express IL-10 receptor. Treatment of primary cortical neurons in culture with IL-10 increased neuronal survival after exposure to oxygen-glucose deprivation (OGD) or glutamate toxicity. IL-10 also induced phosphorylation of AKT in cortical neurons. Pretreatment with the specific PI-3K inhibitor, wortmannin, attenuated IL-10 mediated neuroprotection against OGD and glutamate. In addition, IL-10 induced STAT-3 phosphorylation. Pre-treatment with a functional blocking antibody to the IL-10 receptor reduced both Stat-3 and AKT phosphorylation and blocked IL-10 mediated protection of cortical neurons. These data suggest that IL-10 provides neuroprotection by acting via IL-10 receptor and PI3K/AKT and STAT-3 signal transduction pathways. © 2010 Elsevier B.V. All rights reserved.
Defining the cognitive phenotype of autismT. Charman | C. R G Jones | A. Pickles | E. Simonoff | G. Baird | F. Happé
Volume 1380, Issue , March 2011, Pages 10-21
Although much progress has been made in determining the cognitive profile of strengths and weaknesses that characterise individuals with autism spectrum disorders (ASDs), there remain a number of outstanding questions. These include how universal strengths and deficits are; whether cognitive subgroups exist; and how cognition is associated with core autistic behaviours, as well as associated psychopathology. Several methodological factors have contributed to these limitations in our knowledge, including: small sample sizes, a focus on single domains of cognition, and an absence of comprehensive behavioural phenotypic information. To attempt to overcome some of these limitations, we assessed a wide range of cognitive domains in a large sample (N = 100) of 14- to 16-year-old adolescents with ASDs who had been rigorously behaviourally characterised. In this review, we will use examples of some initial findings in the domains of perceptual processing, emotion processing and memory, both to outline different approaches we have taken to data analysis and to highlight the considerable challenges to better defining the cognitive phenotype(s) of ASDs. Enhanced knowledge of the cognitive phenotype may contribute to our understanding of the complex links between genes, brain and behaviour, as well as inform approaches to remediation. © 2010 Elsevier B.V. All rights reserved.
Spinal muscular atrophy: The role of SMN in axonal mRNA regulationClaudia Fallini | Gary J. Bassell | Wilfried Rossoll
Volume 1462, Issue , June 2012, Pages 81-92
Spinal muscular atrophy (SMA) is a neurodegenerative disease caused by homozygous mutations or deletions in the survival of motor neuron (SMN1) gene, encoding the ubiquitously expressed SMN protein. SMN associates with different proteins (Gemins 2-8, Unrip) to form a multimeric complex involved in the assembly of small nuclear ribonucleoprotein complexes (snRNPs). Since this activity is essential for the survival of all cell types, it still remains unclear why motor neurons are selectively vulnerable to low levels of SMN protein. Aside from its housekeeping role in the assembly of snRNPs, additional functions of SMN have been proposed. The well-documented localization of SMN in axonal transport granules and its interaction with numerous mRNA-binding proteins not involved in splicing regulation suggest a role in axonal RNA metabolism. This review will focus on the neuropathological and experimental evidence supporting a role for SMN in regulating the assembly, localization, or stability of axonal messenger ribonucleoprotein complexes (mRNPs). Furthermore, how defects in this non-canonical SMN function may contribute to the motor neuron pathology observed in SMA will be discussed. This article is part of a Special Issue entitled RNA-Binding Proteins. © 2012 Elsevier B.V.


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Christian Counselor
Michelle Clark, MA, LMFT, Clinical Director
Licensed Marriage and Family Therapist
5279 Kyler Ave. NE Suite 110, Albertville, MN
Christian counseling gives hope to the hopeless and a place to bring the hurt and pain of life. Without Christ we have no place to leave the past and start fresh. When the focus is on Christ and his love for us it helps the healing process and find the joy again created only by having a personal relationship with Jesus Christ. What better way to see ourselves then through the eyes of God the one who created us in his image. He doesn't make mistakes. You are not a mistake! You have worth and value. God created you just the way he needed to to do a job he needed you to do. Together we will discover your purpose and find your strength.
Christian Counselor
Jana Sczepanski Palkert, RN, LMFT
Registered Nurse, Licensed Marriage and Family Therapist
13700 83rd Way North, Suite 201, Maple Grove, MN
I am a practicing Christian and ascribe to the values of my faith. I work with clients of all religious affiliations, and walks of life, and respect our differences. During each intake session, I assess my client's religious preference and desire to incorporate their faith or spirituality into our therapy work. I am open to prayer, talking about God, or other ways to incorporate your spirituality or Christian Faith into therapy.
Christian Counselor
Hanson Associates
Gary D. Hanson, MA, LMFT and Joy A. Hanson, MA, LMFT
7200 Hemlock Ln N - Ste 108, Maple Grove, MN
As graduates of Bethel Theological Seminary, we offer the unique integration of an in-depth Christian worldview and biblically based understanding, with sound research-based clinical practice. Whether you are seeking counsel for emotional or relational struggles from a Christian perspective, or desire to explore your personal faith journey and spiritual goals, we welcome the opportunity to provide a compassionate and sensitive faith-based approach to achieving your goals.
Christian Counselor
Joan Pechauer, LMFT
Marriage and Family Therapist
225 First Avenue NE, Osseo, MN
If you identify yourself as a person of Christian faith, I will integrate lessons from the Bible as we look at what's going on in your life. Jesus had lots to say on our relationships with others and with our Father. When both of these are happening in our lives, we feel peace and harmony. I will help you explore where God's Word can give you direction and will pray with you and for you.
Christian Counselor
Paul Dousi, Phd, LMFT
Licensed Marriage and Family Therapist
6300 117th Ave N., Champlin, MN
The first thing you should know about me is that I am a Christian and that I believe that the Bible is the word of God. Hebrews Chapter 4 and verse 12 says that "...the word of God is living and active..." I believe that this verse is true and help Bible believing Christians understand not only what the Bible says but what it will mean for them to line up their life in accord with it. I do not use the Bible as a weapon but as a gentle guide as I remind people not only about the promises, and power of God but the requirements He has for us. I pray with people and lavish encouragement. Furthermore I give concrete and practical homework so that progress can be made most rapidly.
Christian Counselor
Soul Work Counseling
Licensed Marriage & Family Therapists
11108 Zealand Avenue N, Suite #106, Champlin, MN
Soul Work Counseling uses Christian therapists who have the academic training/professional qualifications to do their work and also base their own lives on Biblical values and truth. We use scripture and prayer in sessions if needed or desired by our clients. Although we have served people of many spiritual backgrounds and beliefs, our Christian clients can especially benefit from the spiritual perspective that we bring to counseling. We believe that our relationship with God impacts our mood, our personality and our relationships in powerful ways, and we use Christian counseling to help our clients find the peace, joy and fulfillment that Christ promises.
Christian Counselor
Vicki Rocha, LPCC
Licensed Professional Clinical Counselor
5820 74th Ave. N. #104, Brooklyn Park, MN
We are a Christian private practice which means we always practice from a Christian value system, but we also have the freedom to explore all issues from a faith standpoint if clients desire to dig deeper. While we have the clinical training, we are all believers and can incorporate scripture, prayer, discussions of faith, and discussions of values into any session. We believe Christ has the power to heal any hurt and provide hope to the hopeless and we strive to demonstrate his love and grace in all of our interactions with clients.
Christian Counselor
Rindie Eagle, MA, LPCC
Licensed Professional Clinical Counselor
450 Jefferson Blvd, Suite 4, Big Lake, MN
The clinic I am associated with happily utilizes Christian counseling when requested. We are all Christians and believe that faith in God is an asset in therapy. Redemption, grace, and forgiveness are healing and can help promote reconnection with your spirituality. The obstacle I most commonly find blocking this path is shame and guilt. Shame grows with secrecy and is impossible to stuff down deep enough without also turning off positive emotions like joy and happiness. My mission is to provide a judgement-free relationship of mutual trust and respect so you feel safe to shine a light on whatever shame or guilt you may have in order to reconnect spiritually and move towards happiness.
Christian Counselor
Kelly Rose, MA, LMFT
Licensed Marriage and Family Therapist
3701 Shoreline Dr, Orono, MN
I have four years of experience practicing Christian based counseling and strongly believe that faith and spirituality are an integral aspect to the healing process. I incorporate spirituality to the course of therapy based on the desired level of my clients. I also incorporate mindfulness, mythology, and other world religions in the treatment process.
Christian Counselor
Rebekah Miller, MA, LMFT
Licensed Marriage and Family Therapist
7575 Golden Valley Road Suite 133, Golden Valley, MN
Do you need a safe place to seek help in a Christian context? You may be struggling with faith concerns, fear of dying, grief, or shame about sin. You may be struggling with problems that are less-clearly related to faith, such as mental health challenges, relationship problems, or family difficulties. I am a Licensed Associate Marriage and Family Therapist with a major in Pastoral Studies. I can address your concerns from the perspective of a professional therapist and a Christian counselor. I will work within your Christian belief system, using Scripture upon request it, but respecting your personal beliefs. Together, we will work to heal relationships and bring grace into each situation.


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- Overview
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Giro Zero GlovesRace-inspired in every way, the Zero gloves provide the ultimate in ventilation, control and bar feel. Pittards Microvent leather and welded mesh panels promote air circulation and wick moisture for a dry experience. Minimalist 3-piece palm construction reduces bunching and allows your hands to move naturally for enhanced control that doesn't compromise bar feel. Sonic-welded pull tab for easy glove removal.
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Complaint Review: MyTech Help, LLC
MyTech Help, LLCInternet United States of America
MyTech Help, LLC Charged our credit card, posing as Apple, requested a refund, transferred us to 4 departments 5 times, hung up on us! Internet
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CARLSBAD: Downtown merchants host dog parade, Santa visits
The annual Pups on Parade , a holiday event for dogs and their owners, is set for Sunday in Carlsbad's downtown Village area.
Hosted by the Carlsbad Village Association , the event includes pictures with Santa in addition to the pet parade.
Pets can pose with Santa from 9 a.m. to noon and from 1:15 to 2:30 p.m. at the Shops at Village Fair at Carlsbad Village Drive and Carlsbad Boulevard. A group photo gathering is planned for 12:30 p.m. in front of the Carlsbad Village Community Tree.
The parade will begin right after the group photo, organizers said.
The photo shoot costs $20 and people will receive a 4-by-6 photo of their dog with Santa as well as a group photo of all the pets in front of the Christmas tree.
Proceeds from the event benefit the Saving Pets One at a Time .


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- Report: #777158
Report - Rebuttal - Arbitrate
Complaint Review: Car Hop
Car Hop10061 Central Ave NE Blaine, Minnesota United States of America
Car Hop Year and a Half and No Title-Car Hop Blames State...State Says NO Way! Blaine, Minnesota
*Consumer Comment: First, GOOD JOB hanging in there and keeping the issue alive.
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Should we just start blaming people who may be down on their luck and lose their job making it impossible to pay their bills on time? How about poor or ill people? How about parents who have spent every dime trying to save their child from cancer? Should we just banish them to a dark corner of society so they dont bother people who are more fortunate? How about the mom who is beaten every day? Should we be blaming her for her bad credit or shattered self-image? Hmm just doesnt seem right does it? Before you blanket judge people, maybe you should find out the whole story. It will save you from looking like a donkeys butt!
Until you have walked a day in my shoes, you have no right to judge me or tell me I should just take it! Furthermore, you have no idea why I had to go to a subprime dealership/loan option, nor should it matter. Below is a point by point story of events
Purchased 1999 Chevy Tahoe 05/2010 from Car Hop, Blaine, MN. Since then have been waiting for a title.
Car Hop contacted me in April and May of 2011 regarding the missing title. Stated there was a discrepancy with the VIN# in the states system and needed to bring it to them to verify.(This was very urgent and requested by the State according to Car Hop). Car Hop mentioned that the state had put a Flag on the account and would not release a title to us until that was cleared.
Car Hop set an appt for Friday 6-03-2011, 3pm at the St. Paul, MN DMV. I said okwhat could I do?
On my time, I took the Tahoe to the DMV for the verification. The DMV stated there is/was no flag on the Tahoe and in fact they have the correct VIN# on file. They continued to state that there was nothing within the States system that needed to be checked or verified and that it was all on Car Hop to take care of any issue preventing a new title to be released.
Called Car Hop (talked with Janelle, Manager at the Blaine car lot where Tahoe was purchased) and made this known to her. She said she would call back.
A week later some man, who offered no title called from the main Car Hop office. I can not remember his name (but do have his number) fed me another story. He said that it was STILL a VIN# mix up and that the state doesnt know their a@$ from a hole in the ground and didnt want to deal with them again.
He insisted that he knew other people that would take care of the title issue. He tried to explain how some numbers were mixed up between owners from different states and that that is why it is taking so long.(really???)
He wanted to take the Tahoe for a day to Glenco MN where he has friends that could get the VIN# mix up straightened out..I said no you are not taking my truck! He said ok and that he would see what else he could do and call me back.
After talking with him I decided to call the state and ask them about the VIN issue and what should or shouldnt be done.
I spoke with Shanice. She stated that they never requested that the car be seen to verify the VIN# and that anything that needed to be done was on Car Hops end. I asked just to verify You never requested that the Tahoe be taken in by me? She stated No and in fact there is no flag on the account. She stated that they are just waiting for the proper forms to be filed so they can release a new title. And as of June 2010 that had not been done.
The mystery man never called, so I called him back. I asked what was going to happen and basically he then changed his story. He told me that through the change of owners/purchases there was a VIN# mix up somewhere within that paperwork that needed to be fixed (this made no sense to me). Since the car was purchased from out of state it would take a few more days to work it out, but he guaranteed me that I would have my title in a couple weeks. I said okwhat could I do? A week later I received a call from Car Hop (Janelle) stating that the St. Paul DMV never faxed the copy of the VIN# verification and they needed to have a copy (not sure why they needed it). Instead of them going to get a copy, they insisted that I drop my copy off to themI said okwhat could I do? Janelle stated this would be the last hoop I needed to jump throughthis was mid-June.
I waited for the title.no title as of today. I called Janelle Sept 8th letting her know there has been no title sent my way yet. She said she would make some calls and get back to me. Late afternoon that day she called back stating that since the government shut down, it would take months to get the title.
I expressed my lack of patients at this point. She stated that the check for the expedited title was cashed by the state, but they refused to rush itso she stated I will just have to wait. I said how longshe didnt know.
I said, well since you have the cashed checkI want a copy as proof. She said I do not blame you, and that she would call me back tomorrow (Sept 9th). In the mean time I thought I would purchase a car fax report. It was interesting.
First offGlenco MN is where Car Hop purchased the Tahoe (Mid-West Auction) so the out-of-state explanation doesnt fly. And it is weird how the mystery man wanted to take the Tahoe to Glencomakes me wonder why?
Before that it was at a Monticello dealer, and before that there are no records. (Not sure if that is normal). What this did solidify for me is the fact that Car Hop has been feeding me one lie after another, stringing me along.WHY? That is the million dollar question.
So I put another call into the state to verify the information from Janelle was accurate (which I already knew wasnt)of course I did find out that it was not.
According to Nick at the St. Paul DMV, there is no record of any request for title transfer from Car Hop, expedited or otherwise. There is no record of any check cashed. I asked about the timeline due to the government shut downhe stated there was no wait. In fact, if a dealer requested and pays for an expedited title, by law they have 3 days to do so.
This means, if they had done what they told meI would have had the Tahoe title many times over by now! He also stated that by law they can not turn away an expedite request. Nor would they cash a check, and then tell the dealership that they are just going to process it in the normal fashion.
However, even if it was not expedited, there is no wait time for any title requested through the mail (which is the way Car Hop would have preceded). I guess the most disturbing information that he told me was that I shouldnt really be driving the truck. The reason is if I were to get into an accident, since I do not have a title in my name I could never claim the insurance money. If, for some reason it would end up in an impound lot, I could never get it back because I do not have a title in my name.
Basically, I am paying on a truck that I do not have any ownership to!
I thank God that nothing has happened as my children travel in the truck as well! Janelle called me Friday Sept. 9th, and to my dismay she stated the only person in the entire company that could get me proof of this check cashed by the state was out of the office until sometime next week.
At this point I just laughedI went on to tell her the information that I obtained from Car Fax and the St. Paul DMV and that she had a couple options. I also told her I want a decision by Monday Sept. 12th or option C would be taken).
a. Get me the title next week.
b. Return the truck to them and have every payment, down payment, and other expenses be reimbursed.
c. Or, if I didnt receive any phone call with option a or b, I would put a complaint into the Better Business Bureau, send in my papers from the MN Attorney generals office and start a personal campaign about the crooked nature of Car Hop to every news channel, news paper, cable networketc
Janelle said she understood why I was so upset and promised she would call back that day.it is Wednesday Sept 14thno one has called me back so I am going with option C
As of Sept 15th the Better Business Bureau of Minnesota has accepted my complaint Case # 57210172 (per Steve F.) and has given Car Hop until Sept 29th to replay with their solution to this title issue. As of Sept 15th I have sent in my forms to the Minnesota State Attorney General Office as they instructed me to do.
Tomorrow, Sept 16th I will be contacting every news organization I can think of along with all newspapers.
If on the 29th of Sept I do not have my title I have an apt with David A. MAHONEY ANDERSON LLC (Business and Internet Law).
This report was posted on Ripoff Report on 09/15/2011 12:42 PM and is a permanent record located here: http://www.ripoffreport.com/r/Car-Hop/Blaine-Minnesota-55434/Car-Hop-Year-and-a-Half-and-No-Title-Car-Hop-Blames-StateState-Says-NO-Way-Blaine-Mi-777158. The posting time indicated is Arizona local time. Arizona does not observe daylight savings so the post time may be Mountain or Pacific depending on the time of year.
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#1 Consumer Comment
First, GOOD JOB hanging in there and keeping the issue alive.
AUTHOR: Ken - (USA)
SUBMITTED: Thursday, September 15, 2011POSTED: Thursday, September 15, 2011
It looks like you may have the issue on the way to resolution. Best of luck to you.
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Tau is a letter of the alphabet in both Hebrew and Greek which represented the totality of a person's life, and came to symbolize the cross of crucifixion. St. Francis of Assisi was especially fond of it as a symbol, signing correspondence with it in place of his own signature. This pressed wood tau cross features an image of St. Francis with the line "Lord, make me an instrument of Your peace," as well as images of Pope Francis and St. Peter's Basilica. Gold detail. Made in Italy.
|Maire (October 30, 2015)
|I ordered one for my home, my husband & I love it so much we ordered one for each of our 4 adult children's homes for a Christmas present.


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Employees at Meridian's temporary city hall got a treat Tuesday. The Northwest Middle School Singers stopped by to sing Christmas carols.
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text:
- Report: #1005085
Report - Rebuttal - Arbitrate
Complaint Review: Grand Crowne Resort At Pigeon Forge
Grand Crowne Resort At Pigeon Forge222 Whistling Wind Way Pigeon Forge, Tennessee United States of America
Grand Crowne Resort At Pigeon Forge The Lodges At the Great Smokey Mountains I can't believe I fell for this...run away and don't believe them Pigeon Forge, Tennessee
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The salesperson was tammy tarver. She was telling us how much better this was than a time share. Bragged about the platinum status and how we were going to get 12 getaway weeks plus our points which would give us 15 weeks a year to enjoy. If we couldn't enjoy them ourselves we could rent the weeks to help pay the timeshare off earlier and enjoy the income. She also told us about this wonderful vacation her and her family took to disney world. Said she stayed ON DISNEY at the ANIMAL KINGDOM MOTEL for $169 dollars a week per room. Well, that sold me. MY family are big disney fans so that sold me quickly.
I didn't know people could lie so much to you in an open meeting but I later learned everything they tell you are lies. Mrs. tammy even promised us she would personally help us rent our weeks out so we wouldn't have to go through the services and pay more money. so we agreed to the purchase thinking all the time if it sounds to good to be true........how sweet it was to good to be true. .
We went from being so excited to crushed not only did we give them a $1500 deposit but we had to pay fees for maintaince a few months into the purchase. It took them till late feb to get us our paper work. We were trying to set up a close getaway week with our weeks and trying to set up renting our weeks and were told we had to be members for 1 year before we could use the weeks. we were also told later you can't rent the get away weeks. Only the regular weeks.
Oh and guess what....there isn't anyway to use this wonderful program to stay on disney. So....let me see.
I have purchased a stupid piece of paper that isn't worth anything for 14,000 dollars. We have tried to contact anyone we can and no one can help. They all say something differant. All we want is out of this stupid thing.
We were going to stop paying then we started getting harrassing phone calls about the payments have nothing to do with the time share. Its someone differant that financed and they would go after us if we don't pay.
WE NEVER EVER HAVE BEEN ABLE TO GET A WEEK, A FEW DAYS, HECK EVEN A DAY IN ANY RESORT. Every time we try there isn't anything available. I even tried a year out. Nothing!!!!! so please people run run run away from this no discount tickets are worth it. I so wish someone would step in and shut them down and give everyone refunds for all there heartache. I haven't been back but I would bet there isn't anymore cabins built but the three that was there when we bought.
Oh yes one more thing WE bought in Pigeon Forge but we are deeded in Branson. They said if we wanted to change that we had to pay more. It never ends....run far far away. I really hope this helps someone. Wish i had read something like this before my misfortune.
This report was posted on Ripoff Report on 01/28/2013 06:29 PM and is a permanent record located here: http://www.ripoffreport.com/r/Grand-Crowne-Resort-At-Pigeon-Forge/Pigeon-Forge-Tennessee-/Grand-Crowne-Resort-At-Pigeon-Forge-The-Lodges-At-the-Great-Smokey-Mountains-I-cant-beli-1005085. The posting time indicated is Arizona local time. Arizona does not observe daylight savings so the post time may be Mountain or Pacific depending on the time of year.
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Test our elected officials
Published: Friday, August 1, 2003 at 6:01 a.m.
Last Modified: Friday, August 1, 2003 at 12:26 a.m.
There has been much interest recently in testing students, from kindergarten through the university level. To those proposing standardized testing, the tests themselves seem to be the panacea to "fix" educational problems and to ensure some vague measure of accountability.
The motivations of those demanding testing, the validity of their premise and solution and their qualifications to make these demands, seem woefully under-examined.
However, as I pondered the problems facing the local municipal, state and federal governments, and as I have watched the antics of legislators and administrators in agencies, legislatures and Congress, I, too, have become an advocate of testing.
In that vein, I offer a modest proposal. Every individual considering running for elected office, from county commissioner to president of the United States, and every high-level nominee for appointed office (for example, judges, bureau heads, Cabinet appointees) should be tested
The tests should cover six areas: law, government, history (national, state or local), economics, natural resources, science and environmental function, and human societies.
Scores should be published by the news media, and the various "leadership" teams given letter grades, from A (outstanding) to F (failure).
Although it might not be possible to exclude an individual from running for office (say, for constitutional grounds), at least the voting public would know how well the candidates or officials scored in the most basic areas of knowledge related to public office of high government service.
Surely, if the persons advocating universal testing for students deem it a meritorious way to measure future promise and success, the public has a right to know the level of basic competency of those legislators and officials who make such critical decisions affecting the everyday lives of the public and the biosphere on which we all depend.
If universal testing for basic skills and subject matter understanding was mandated for city hall, Tallahassee, and Washington, perhaps we would not have some of the bone-headed decisions and embarrassing votes from which we (and our children) will suffer from for years.
Anybody with me?
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