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Chronic sleep deprivation in mice with Alzheimer's disease-type changes makes Alzheimer's brain plaques appear earlier and more often, researchers led by Cure Alzheimer's Fund's Dr. David M. Holtzman at Washington University School of Medicine in St. Louis reported in Science Express. The study was funded in part by Cure Alzheimer's Fund.
They also found that orexin, a protein that helps regulate the sleep cycle, appears to be directly involved in the increase. Neurodegenerative disorders like Alzheimer's disease and Parkinson's disease often disrupt sleep. The new findings are some of the first indications that sleep loss could play a role in the genesis of such disorders.
"Orexin or compounds it interacts with may become new drug targets for treatment of Alzheimer's disease," says senior author Holtzman, the Andrew and Gretchen Jones Professor and chair of the Department of Neurology at the School of Medicine, and neurologist-in-chief at Barnes-Jewish Hospital. "The results also suggest that we may need to prioritize treating sleep disorders not only for their many acute effects, but also for potential long-term impacts on brain health."
Holtzman's laboratory uses a technique called in vivo microdialysis to monitor levels of amyloid beta in the brains of mice genetically engineered as a model of Alzheimer's disease. Amyloid beta is a protein fragment that is the principal component of Alzheimer's plaques.
Jae-Eun Kang, Ph.D., a post-doctoral fellow in Holtzman's lab, noticed that brain amyloid beta levels in mice rose and fell in association with sleep and wakefulness, increasing in the night, when mice are mostly awake, and decreasing during the day, when they are mostly asleep.
A separate study of amyloid beta levels in human cerebrospinal fluid led by Randall Bateman. M.D., assistant professor of neurology and a neurologist at Barnes-Jewish Hospital, also showed that amyloid beta levels were generally higher when subjects were awake and lower when they slept.
To confirm the link, Kang learned to use electroencephalography (EEG) on the mice at the Sleep and Circadian Neurobiology Laboratory at Stanford University with researchers Seiji Nishino, M.D., Ph.D., and Nobuhiro Fujiki, M.D. Ph.D. The EEG readings let researchers more definitively determine when mice were asleep or awake and validated the connection: Mice that stayed awake longer had higher amyloid beta levels.
"This makes sense in light of an earlier study in our lab where John Cirrito, Ph.D., showed that increases in synaptic activity resulted in increased levels of amyloid beta," Holtzman notes. "The brain's synapses may generally be more active when we're awake."
Depriving the mice of sleep caused a 25 percent increase in amyloid beta levels. Levels were lower when mice were allowed to sleep. Blocking a hormone previously linked to stress and amyloid beta production had no effect on these changes, suggesting they weren't caused by the stress of sleep deprivation, according to Holtzman.
Researchers elsewhere had linked mutations in orexin to narcolepsy, a disorder characterized by excessive daytime sleepiness. The brain has two kinds of receptors for orexin, which also is associated with regulation of feeding behavior.
When Holtzman's group injected orexin into the brains of the mice, mice stayed awake longer and amyloid beta levels increased. When researchers used a drug called almorexant to block both orexin receptors, amyloid beta levels were significantly lower and animals were awake less.
Miranda M. Lim, M.D., Ph.D., a neurology resident and post-doctoral researcher in Holtzman's lab, performed long-term behavioral experiments with the mice. She found that three weeks of chronic sleep deprivation accelerated amyloid plaque deposition in the brain. In contrast, when mice were given almorexant for two months, plaque deposition significantly decreased, dropping by more than 80 percent in some brain regions.
"This suggests the possibility that a treatment like this could be tested to see if it could delay the onset of Alzheimer's disease," says Holtzman.
Holtzman notes that not only does the risk of Alzheimer's increase with age, the sleep/wake cycle also starts to break down, with older adults progressively getting less and less sleep. Investigators are considering epidemiological studies of whether chronic sleep loss in young and middle-aged adults increases risk of Alzheimer's disease later in life. Holtzman also plans to learn more of the molecular details of how orexin affects amyloid beta.
"We would like to know if there are ways to alter orexin signaling and its effects on amyloid beta without necessarily modifying sleep," he says.
Additional studies will address the questions of whether increased amyloid beta during wakefulness is connected to increased synaptic activity and whether some aspect of sleep lowers amyloid beta levels independent of synaptic activity.
Vaccination against amyloid is a promising approach for the development of Alzheimer's disease (AD) therapeutics. Approximately half of the investigational new therapeutics in human clinical trials for AD are active or passive immunotherapeutics.
Active vaccination involves the injection of an antigen and relies on the production of antibodies in the vaccinated patient. Four human clinical trials of active vaccination currently are under way. Passive immunization is also a promising strategy that involves the production of antibodies outside of the patient and injection of these antibodies. There are currently 12 clinical trials of passive immunization. You can check for Alzheimer therapeutics in human clinical trials by visiting www.clinicaltrials.gov and searching for key words "Alzheimer's and immunotherapy."
The development of vaccinations as a strategy for treating or preventing Alzheimer's is an example of thinking out of the box. Vaccinations commonly are associated with infectious diseases, like influenza, small pox and polio, which appear to have little in common with neurodegenerative diseases, like Alzheimer's. Moreover, the brain is an immunoprivileged site with little access to antibodies, so it seems unlikely antibodies would be protective in the brain.
Researchers were pleasantly surprised when Dale Schenk and co-workers at Elan Inc. reported that vaccination of transgenic mouse models of AD against the amyloid Aß peptide prevented amyloid deposition in young animals and removed pre-existing amyloid deposits in older animals. Subsequent work showed that immunization against Aß prevented or reversed many other pathological features and prevented cognitive dysfunction in transgenic mice and non-human primates. This vaccine (Elan AN1792) was tested in human clinical trials, where it showed similar beneficial effects of removing amyloid deposits and slowing cognitive decline in patients with significant levels of anti-Aß antibodies, but the clinical trial was halted because 6 percent of the patients developed meningoencephalitis, an inflammatory side effect.
To circumvent the unwanted inflammatory side effects, second-generation active vaccines have been developed and passive immunization strategies have been explored. The second-generation vaccines use small pieces of the amyloid Aß sequence to avoid activating the T-cells responsible for meningoencephalitis, while passive immunization bypasses the human immune response by directly supplying antibodies. These newer strategies have shown the same beneficial effects in transgenic mice and passive immunization has shown some promise in a subset of patients in human trials, but they have raised new questions about their effectiveness and potential new side effects. Elan/Wyeth reported preliminary results from clinical trials of their monoclonal antibody, Bapineuzimab, that demonstrated only a small benefit in a subgroup of patients who lack the apoE4 genotype. They also failed to observe an improved benefit with an increased dose of antibody and reported side effects, like a buildup of fluid in the brain. Results of active vaccination human clinical trials with second-generation vaccines remain to be reported.
Both second-generation vaccines and antibodies suffer from a common problem. They both target linear amino acid sequences found in normal human proteins (the amyloid precursor protein) and in the amyloid deposits themselves. Making antibodies against normal human proteins can cause autoimmune side effects, in which the immune system is attacking normal human cells in addition to the Alzheimer's pathology. Fortunately, it is difficult to make antibodies against self-proteins because of immune suppression of auto antibodies. Third-generation vaccines seek to overcome these problems of autoimmune side effects and autoimmune suppression by using antibodies that target structures specific to the amyloid aggregates and that do not react with normal human proteins.
Cure Alzheimer's Fund has been supporting two projects that seek to develop third-generation immunotherapeutics. Dr. Charles Glabe's laboratory is developing active vaccines and monoclonal antibodies that recognize conformations of the amyloid peptide that only occur in the pathological amyloid oligomer aggregates, while Dr. Rob Moir's lab is working on cross-linked amyloid peptides (CAPs) that are only found in disease-related aggregates. Dr. Glabe's strategy relies on the fact that when the Aß peptide aggregates into ß-sheet oligomers, it creates new antibody recognition sites, known as epitopes, that are not found on native proteins. The surprising finding is that these oligomer-specific antibodies recognize amyloid oligomers from other diseases that involve amyloids formed from sequences unrelated to Aß. This means the same antibodies also may be effective for other amyloid-related neurodegenerative diseases, like Parkinson's disease.
The explanation for why the antibodies are specific for amyloid oligomers that involve several individual peptide strands arranged in a sheet and yet recognize these sheets when they are formed from other amino acid sequences is simple and elegant (Figure 1). It is now known that most pathological amyloids aggregate into simple and very regular structures where the peptide strands are arranged in parallel and where the amino acid sequence is in exact register. This is like a sheet of paper upon which the same sentence is written on each line. The individual amino acids line up and down the sheet in homogeneous tracts, known as "steric zippers." The steric zippers do not occur in normal protein structures and the oligomer-specific antibodies are thought to recognize these steric zipper patterns on the surface of the sheets. Since all proteins are made up using the same 20 amino acids, any sequence in this parallel, in-register structure gives rise to the same steric zippers regardless of the linear sequence, which can explain why the antibodies recognize the oligomers formed by different proteins.
Dr. Moir's group is working on CAPs, where Aß is cross-linked by oxidation of a tyrosine residue at position 10 of the peptides' sequence. Aß is oxidized after it is produced from the amyloid precursor protein as a consequence of the abnormally high level of oxidative activity in a brain with AD and the peptides' propensity to bind redox active metals. Excessive CAPs generation is associated with the disease state and is not a normal feature of Aß biology. The cross-linking at tyrosine 10 that gives rise to CAPs may serve to align the peptides in a parallel, in-register fashion and promote the generation of still-larger oligomeric aggregates that display steric zippers on their surface.
Dr. Moir and Dr. Rudy Tanzi's labs found that natural antibodies to CAPs are reduced in the blood of patients with AD. More recently, evidence published by Tony Weiss-Coray's group at Stanford University supports the idea that antibodies that recognize steric zippers and CAPs may be important for protecting against Alzheimer's disease. The levels of these antibodies that target the zippers and CAPs were among the highest in young, normal humans; levels dropped with aging and with AD. Furthermore, the results of a recent study supported by Baxter Biosciences of patients that received human antibodies purified from normal individuals (IVIg) reported that antibody treatment reduced the risk of being diagnosed with AD by 42 percent over the five-year study period. This is one of the most remarkable reports of prevention of AD by any therapy. Although the normal human antibodies that target amyloid primarily recognize the steric zippers and CAPs, these antibodies are present at relatively low levels. It is reasonable to imagine that an even greater protective effect might be achieved by boosting the levels of these protective antibodies by either active vaccination or passive immunization.
Figure 1 shows how the same steric zipper patterns are formed on parallel, in-register oligomers from completely different sequences. A segment of the Aß sequences is shown in the upper left corner and a random sequence is shown in the upper right. Each amino acid is designated by a capital letter. Typical antibodies recognize the linear sequence (from left to right) indicated in the horizontal boxes, which is unique to each sequence. When the peptides aggregate to form pathological oligomers, they line up in a parallel, in-register fashion, shown below. This gives rise to steric zippers that run up and down the sheet perpendicular to the sequence, shown in vertical boxes. Aggregation-dependent, disease-specific antibodies recognize the steric zippers from many different amyloid sequences. Zippers from F and V amino acids are shown in boxes, but there are potentially 20 different zippers; one for each of the 20 amino acids.
The fact that a completely random sequence can form the same type of steric zipper as is found in Aß amyloid in Alzheimer's disease means we can use a non-human, random peptide sequence as a vaccine to produce a protective immune response that has a very low potential for autoimmune side effects. Vaccines based on non-human peptides, like diphtheria and pertussis toxin, are so safe they routinely are given to infants. There is no reason to expect that a vaccine for AD that targets the disease-specific steric zippers wouldn't be as safe and free of side effects. A goal of the research funded by Cure Alzheimer's Fund is to do the preclinical investigations that are a necessary prelude to getting these third-generation vaccines and monoclonal antibodies that target disease-specific epitopes into human clinical trials.
This Science Update gives you an overview about what is know about the science behind Alzheimer's disease and how at Cure Alzheimer's Fund we are funding research to get to a cure as quickly as possible.
Download the document >
A brief summary of important potential treatments and CAF's related research.
Cure Alzheimer's is funding the management and continued development of a revolutionary web based database.
There has been a spate of announcements about promising drug therapies, "new" genes and environmental factors affecting Alzheimer's disease (AD) in the news lately. These are likely to increase as the media becomes more sensitized to the looming disaster that Alzheimer's presents to the world. We thought it would be useful to bring you up to date on our research agenda. Cure Alzheimer's Fund's supported research is active in basic genetic research and early stages of drug development, and also addresses several key environmental factors.
From an article in Medical News Today about a paper recently released in the journal Neuron, June 7, 2007:Researchers from the MassGeneral Institute for Neurodegenerative Disorders (MGH-MIND) have discovered how brain cells affected by stroke or head injury may cause generation of amyloid-beta protein, which is a key factor in the Alzheimer's disease story.
Cure Alzheimer's Fund's core research effort continues to be the Alzheimer's Genome Project™ initiative. Using whole genome association to analyze DNA, the objective is to identify all the genes that affect risk for AD. That project, largely based at Massachusetts General Hospital and Harvard Medical School, continues and is on time for completion by summer of 2008.
The core research effort currently funded by Cure Alzheimer's Fund is the Alzheimer's Genome Project™ initiative. This project, entirely funded by Cure Alzheimer's Fund, is being led by Dr. Rudolph Tanzi at Massachusetts General Hospital. The objective is to identify all genes that contribute significant risk for Alzheimer's disease, thereby identifying more targets for the development of therapeutic interventions.
By Charles Glabe, Ph.D. University of California at IrvineProfessor, Molecular Biology and Biochemistry, School of Biological Sciences.
The current treatments for AD target the disease symptoms and to prevent or cure AD, new treatments are needed that target the causes of the disease. Aß oligomers are a leading candidate for causing AD, so it makes sense to develop strategies to prevent their formation, promote their elimination or inhibit their toxic activity.
Alzheimer's disease (AD) is the most wide spread and debilitating disease that robs otherwise healthy individuals of essential functions, such as memory and cognitive ability. One of the critical aspects of AD is accumulation of misfolded proteins as deposits in regions of the brain involved in learning and memory that are known by the general term "amyloid". One of the curious aspects of amyloid is that it also accumulates in other degenerative diseases associated with aging, like Parkinson's and Huntington's diseases and type II diabetes. In AD, the amyloid deposits are primarily made up of a small protein known as "amyloid beta", or Aß, while in other degenerative diseases a different type of protein forms the amyloid. In most of these diseases, mutations in the amyloid forming protein promote the misfolding of the protein and are associated with rare inherited forms of disease, providing strong evidence that amyloid formation is closely linked to the disease.
Amyloids grow into long, thin fibrils by the addition of misfolded proteins on to the ends much like the addition of a single Lego block on to a stack. Proteins are linear strands of amino acids that fold into complex globular shapes that are critical for the proteins function. In order for a normal protein to form an amyloid fibril, it must undergo a change in its original shape from a globular form to an unwound abnormal shape that allows it's self-assembly with other misfolded protein strands like Lego blocks. This assembly can go on infinitely, so that each amyloid fibril may contain a million or more individual subunits or blocks. Although amyloid accumulation is a key feature of AD, it also presented an enigma because the accumulation of insoluble amyloid fibril deposits is poorly correlated with dementia. Some cognitively normal individuals were found to have the same amount of insoluble amyloid deposits as AD patients, indicating that these deposits are not always associated with disease. Similarly, other AD patients have been observed with relatively little of the insoluble amyloid deposits. These observations refocused research away from the insoluble amyloid deposits to other types of amyloid aggregates known as "oligomers". More recent research in amyloid aggregation has discovered that the amyloid formation pathway also includes smaller aggregates, or oligomers and these oligomers have a different shape or conformation of the protein than that found in amyloid fibrils. Like Duplo blocks and Lego blocks, the oligomer conformation does not co-assemble with the fibril building blocks, but rather only supports the self-assembly of small aggregates of about 3-24 individual peptide strands. Amyloid oligomers have been observed for AD and other amyloid-related degenerative diseases. There is increasing evidence that these small oligomers, rather than the long fibrils, are the primary toxic or pathogenic species that cause all of these degenerative diseases. Oligomers are more toxic to cells and their presence correlates better with disease than the fibrils. Determination of the structures of these toxic oligomers, what they do to cause disease and how we may prevent their toxic activity are the primary objectives of Cure Alzheimer's Fund Research Consortium Collaborative.
The Cure Alzheimer's Fund Research Consortium Collaborative consists of five of the members of the Research Consortium and a member of the Cure Alzheimer's Fund Science Advisory Board. This highly innovative collaborative project investigates critical aspects of amyloid oligomers in AD. The project is in it's second year of funding.
For a full summary of the funded researchers and their projects, please visit our website www.curealzfund.org and see the The laboratories of Dr. Charles Glabe, University of California at Irvine, and Dr. Virginia Lee, University of Pennsylvania, are making monoclonal antibodies that specifically recognize distinct types of amyloid oligomers. These properties of specific antibodies are very important for the development of passive immunotherapy and vaccines for AD, which is one of the leading strategies for therapeutic development (see "A Vaccine for Alzheimer's disease?" by Dr. David Holtzman in the Fall 2006 quarterly report for more details about vaccine development.) Oligomer specific monoclonal antibodies are also useful for screening for drugs that prevent oligomer formation and as diagnostic agents. Although diagnostic agents may not seem to have much utility until better treatments are available for AD, they are critical for developing new therapies by allowing clinicians to recruit more homogeneous populations of individuals at risk for disease onset for human clinical trials. They are also crucial for drug development by allowing pharmaceutical companies to directly evaluate the effectiveness of drugs that target amyloid oligomers.
Drs. Rudy Tanzi and Robert Moir of Massachusetts General Hospital/Harvard Medical School are working on the discovery of drugs that prevent the formation of a novel type of amyloid oligomer knows as "cross-linked amyloid protein species" (CAPS). These results suggest that immunization with anti-CAPS antibodies and drugs that prevent the formation of CAPS might provide therapeutic benefit for AD. Drs. Tanzi and Moir are also providing CAPS to other members of the Cure Alzheimer Fund research consortium for analysis of their immunological properties and toxic activity.
Drs. Sangram Sisodia, University of Chicago, and Sam Gandy of Mt. Sinai Medical School are working on amyloid oligomers in transgenic mouse models of AD. Dr. Sisodia's laboratory is working on Aß*56, a particular type of amyloid oligomer that is closely associated with the development of cognitive dysfunction in Tg2576 mice. Dr. Sisodia's lab focuses on the molecular analysis of Aß*56 structure and function and how exercise may impact the formation of Aß oligomers. Dr. Gandy's laboratory is developing new transgenic mouse models of AD that have different types of amyloid oligomers and these animal models will be shared with other members of the consortium. These animal models are very important for development of new therapeutics because they provide a means of determining the pathological significance of amyloid oligomers and they can be used for testing new drugs and vaccines for effectiveness.
Drs. Paul Greengard of The Rockefeller University, David Holtzman of Washington University at St. Louis and Dr. Tae-Wan Kim of Columbia University Medical Center are investigating the relationship between oligomers and neuronal synapse function. Synapses are critical for neuronal communication in learning and memory and there is evidence that synaptic loss and dysfunction play a role in AD.
Why target Aß oligomers?
The current treatments for AD target the disease symptoms and to prevent or cure AD, new treatments are needed that target the causes of the disease. Aß oligomers are a leading candidate for causing AD, so it makes sense to develop strategies to prevent their formation, promote their elimination or inhibit their toxic activity. Vaccination against Aß has shown considerable promise in human clinical trials, but one of the hurdles that must be overcome in order to develop an effective vaccine is to develop vaccines that lack undesirable inflammatory side effects. Vaccines that specifically target the misfolded conformation specific to amyloid oligomers may eliminate oligomers or block their toxicity and overcome these side effects. Since the structures recognized by the antibodies are specific for the disease state and do not recognize the normal, non-disease related protein structures, vaccination against the oligomeric conformation may be less likely to cause inflammatory complications. Conformation dependent monoclonal antibodies may be more effective therapeutic agents because they bind only to the pathological oligomers that are present at low concentrations and will not bind to amyloid plaques. Similarly, drugs that specifically target Aß oligomer formation or toxicity may be more effective because lower concentrations of drugs may be needed to achieve a therapeutic benefit and they may have lower side effects as a consequence. The Cure Alzheimer's Fund Research Consortium Collaborative has a broad and integrated research program that is focused on developing therapeutic agents that prevent or cure AD by targeting the cause of AD.

subset: commoncrawl


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Here's a little background about me:
In high school I was the quiet nerdy girl that had no friends. I'm not sure how I ended up in that role, but it's where I spent my whole four years of high school. I was also rather unfortunate looking.
Now I'm in college. I'm in my junior year, though I've taken extra credits so I can graduate early. I'm studying Psychology and American History at a prestigious university. I come from a lower class family and received a large scholarship. I have already been offered a scholarship that would cover my grad school program completely. At the moment, school is everything.
I work two jobs to support myself. One is in a bar, where I work with many other students. My other job is as an account executive to a cosmetics company, where I am the youngest employee by 20 years. I work 30 hours a week.
In my free time I write (I'm currently working on a novel), take pictures (I'm taking a photography class next semester), and train for Tae Kwon Do (I'm an orange belt). I spend most of my time in coffee shops, bookstores, cafes, and art museums.
As far as looks go, I have shoulder length auburn hair that is usually wavy, though I straighten it sometimes. I wear minimal makeup, but always a little to enhance my looks. I dress like a normal college student, though sometimes I like to dress up in cocktail dresses. I am 5'5", wear a size 4 jeans and size 2 dress, and have a 32B chest size.
After reading all that, could you please tell me what I'm doing wrong? I've never had a guy approach me before. I've never been flirted with or asked out on a date. I have approached guys before, but they always brush me off. Could you please tell me what to change, or give me helpful advice on getting guys to notice me or accept my date offers?
Why can't I get a date? Am I doing something wrong?
Here's a little background about me:
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What Guys Said 1
not to be mean but the problem is that your not overly interesting so your not going to draw the attention of most guys from other girls. you've gotta get some new hobbies that are exciting and can showcase a fun side of you. clubbing for example get out there and talk to guys with some confidence and you might have better luck00|00|0
is their anything besides clubbing that would make me more interesting? I hate drinking and partying.
umm well you cut out a lot of the things I do for fun to meet people.. maybe join a gym or something just saying that writing books and photography and working a lot is nice to see that you can support yourself but isn't going to attract guys. You've gotta go out of your comfort zone so perhaps you should try to like drinking and partying
What Girls Said 1
I think your interests and hobbies are very interesting. don't change your interests or hobbies just to get a guy. that is so ridiculous! have confidence in yourself. flirt with your eyes and a smile. act interested in guys. :)10|10|0
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Most Helpful Guy
I haven't, but my brother has. The last house we lived in had a breezeway. One night he walked into it, and out the window to his left he saw a bright glowing orange orb hovering ten feet off the ground. Keep in mind that the only thing one normally sees in that window is our back yard, some trees, and then a corn farm.00|00|0


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School open
St. Bernard's Elementary
P.O. Box 70
Witless Bay, NL
Telephone: 334-2222
Facsimile: 334-2333
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English School District
eastern Regional Office
Suite 601, Atlantic Place
215 Water Street
St. John's, NL A1C 6C9
Tel: (709) 758-2372
Fax: (709) 758-2706
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- St. Bernard's Elementary Website
St Bernard's Elementary is a school of approximately 350 students located on the beautiful Southern Shore. Our school offers learning opportunities for students from kindergarten to grade six. We are proud to serve the communities of Bay Bulls, Witless Bay, Mobile, Tors Cove, Burnt Cove, St. Michael's and Bauline.
Students that come to St Bernard`s benefit from a fantastic learning environment and an enriched curriculum. We are proud of the many partnerships that have been developed with organisations to ensure that our students have a wonderful learning experience. Enjoy exploring our school website, we would love to hear from you!
Region: eastern
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Grade Level: Kindergarten - Grade 6
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Angy C Model
KODEC PhotographyPhotographer Male Brasschaat, Antwerp, Belgium
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About MeI am a part time professional photographer who specializes in black and white artistic nude photography. For twenty years I was lighting designer for a modern dance company in Belguim and now work primarily with dancers and gymnast. For me nothing in the world is more satisfying than taking a perfect picture of a beautifully lit human body.
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You may not know it from my reviews or forum interactions, but I can be a real asshole sometimes. Hell, I already had this review half-written in my mind before even hearing a single note: a rant on the ever-cheapening meaning of the phrase "rock n' roll", and a snarky simile comparing the use of the "blackened" descriptor in music to its use in Cajun cooking. Another paragraph to prove my points, a witty conclusion, and I could call it a day.
Thanks for ruining my plans, Maax.
In reality, I could still do the above, but they just wouldn't be the same with a positive twist. Maax does indeed rock and roll, just like Motorhead; they are also blackened, much like Venom, although maybe a bit burnt in the vocal area. Considering that Cronos, Mantas, and Abaddon themselves surely borrowed a thing or two from Lemmy, Philthy, and Fast Eddie, adding a few shades of evil to that high-octane rock swagger isn't an entirely foreign concept. True to form, then, that Unholy Rock N' Roll produced many a flashback to Venom's debut – and not just because "Do What thou Wilt" seems to have lifted the main riff from that album's title track. It almost comes as a surprise, since things lean more towards the darker death / thrash side at the outset. But when the chant of "We don't give a fuck!" breaks out during the title track, you know you've just been flipped (off).
It may just be the similarity to "Welcome to Hell" but "Do What Thou Wilt" is ridiculously good, so much so that it bears repeating, apparently. The more rockin' Venom-isms continue through the eponymous "Maax" and "Rot and Roll" before taking a heavier turn with "Overthrone" and "Black Thrash 'Em All," and then evening out for the final two tracks. All the while, Maax never sounds contrived or rehashed. Their influences come through loud and clear, but not in a way that comes off as simply aping them, rather that they identify with them and are just trying to continue down the road that they paved.
Maax prefers their metal to be rebellious rather than Satanic, and having exchanged the latter for the former, they keep the whole rocking, twisted, evil vibe without the over-the-top lyrical content. Part of their bio states "WE ARE HEAVY METAL," eschewing finicky sub-genre labeling for simple truth. Check them out and rediscover all that you loved about this music in the first place.


text:
one of my extra grips for my PX4 is cracked?
I own a px4 in 9mm and i never changed the grip because i felt that the one that came on it fit well enough. but then i thought id get a feel for the large back strap and when i pulled it out of the box i noticed it was cracked a couple mm on the side. is this something that beretta would be willing to replace for me at no charge? ive never had to deal with manufacturers so i dont know what to expect. its never been used and i never took it out of the box until recently.
How long ago did you buy it? I would think it's worth a shot to call Beretta and plead your case.
i purchased it in june i think. but yes i will call and plead my case of course.
Only way to answer your question is to call Beretta. If you get no help post your request, maybe some one will sell you or give you their unused back strap.
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text:
COLOURFUL flowers were on show in Wotton at the weekend's spring show.
Wotton-under-Edge Gardening Club's annual spring flower show took place in the Baptist Church Hall on Rope Walk on Saturday, April 12.
The event is smaller than the club's main autumn show and does not carry produce or food classes, instead focussing on the beautiful blooms that abound at this time of year.
Show organisers said the show had proved popular, with over 100 entries and 60 visitors in addition to the club's own members.
Club chairman David Wilson said all the plants on sale had been snapped up and the steady flow of people during the day had made for a surprisingly relaxing atmosphere.
He said there had been a wonderful selection of locally-grown flowers on show.
"I was very surprised that there were so many daffodils considering the weather has been so mild," he explained. "I think we just hit the right weekend when the daffodils were ending and the tulips starting."
Kate Tucker was the overall winner with the most points across various classes, while Marian Burrows scooped the best exhibit for a magnificent vase of daffodils, featuring 30 to 40 stems, including different varieties of the flower.
The club's premier autumn show and plant sale will be in the town hall on Saturday, September 13, featuring vegetables, fruit, flowers, plants and cookery classes.


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HR0160 – Termination of Employment
|Termination Categories
|Related Policies
|Termination Codes
To identify the types of terminations and establish termination categories for university employees.
- When termination of employment becomes necessary, whether employee or employer initiated, proper procedures must be followed to assure equitable treatment to all parties. Termination from the University of Tennessee shall be officially documented in such a manner as to establish a clear record of action, both as a service to the terminating employee and to the university. An employee will be terminated on his or her last working day except when termination occurs while the employee is on leave of absence without pay (see POLICY HR0355, LEAVE OF ABSENCE) or if the exceptions as stated in POLICY HR0320, DAYS OF ADMINISTRATIVE CLOSING; POLICY HR0338, FAMILY AND MEDICAL LEAVE and, POLICY HR0350, HOLIDAYS, apply. If appropriate, unused annual leave,not to exceed the allowable maximum, will be paid as a lump sum in the employee's last pay check.
Termination Categories[top]
- There are several categories of termination recognized by the university. When initiating the termination papers, the categories will be identified by use of the termination codes as explained in this policy.
- Resignation. The employment relationship is most typically severed by employee resignation. This is a voluntary action on the part of the employee. The absence of an employee without notification for three days, also known as a "Voluntary Quit," and the absence of an employee due to "Inability to Work" are each categorized as a resignation.Staff members are expected to notify their immediate supervisor in writing of their intention to resign their employment. Faculty will follow the policy as established in the applicable faculty handbook. Staff non-exempt employees are expected to give a minimum of two (2) weeks notice and staff exempt employees are expected to give a minimum of four (4) weeks notice. Whenever possible, reasonable advance notice of an employee's resignation is expected. Supervisors should acknowledge and accept the resignation in writing.
- Discharge. This is an action initiated by the employer to terminate an employee. Such terminations will strictly adhere to the university DISCIPLINARY ACTION POLICY AND PROCEDURES. The discharge of a staff member is an action to be taken with extreme care to assure protection to all parties concerned. Supervisors shall contact their campus human resources office prior to discharging any employee to ensure that such action is appropriate and consistent with university policy. No discharge is considered effective if the human resources officer determines that university policy has not been followed.
- Reduction in Force. A campus or unit may have to institute reductions in force. This is an action by the employer to terminate an employee or employees because of temporary or permanent lack of work, lack of funds, or reorganization.
- Death
- Non-Reappointment. This is an action initiated by the employer to terminate a faculty member who is not recommended for reappointment to an academic rank. The policy and procedures to be followed are delineated in the applicable faculty handbook.
- Retirement. This is the termination of employment by an employee who is retiring. Staff employees are expected to notify their immediate supervisor in writing of their intention to retire and the date of expected retirement. Copies of this retirement notice shall be sent to the employee's human resources office. Faculty will follow the policy as established in the applicable faculty handbook.
- Student Termination. This is the termination of employment of a student employee for any reason other than Discharge.
Termination Codes[top]
- The following termination codes will be used when initiating terminations:
- Resignation
100 To accept employment at another college or university (Code 105 has priority.) 105 To accept employment with a State of Tennessee agency or State Board of Regents institution 110 To accept employment in industry or other 120 To further education 125 Completion of educational work requirements 130 Illness or injury or medical disability 135 Inability to work 140 Quit without notice; abandonment of position 150 Family obligations 160 Moving out of area (Codes 100 thru 120 have priority.) 170 Failure to return from leave of absence 180 Working conditions 185 Dissatisfaction with job 190 No longer desires work (Codes 100 thru 185 have priority.) 195 * Not eligible to work due to policy or regulations (Visa, I-9, etc.)
- Discharge
205 * Inability to meet performance standards (inadequate work performance) 215 * Refusal to follow clear instructions (termination for cause) 225 * Gross misconduct 235 * Employee error that is threatening to life or could result in significant property loss 240 * Violation of university work rules 245 * Excessive absenteeism or tardiness 275 * Termination during probationary period 290 * Court-ordered termination
- Reduction In Force
300 * Laid-off--Lack of work 310 * Laid-off--Lack of funds 320 * Laid-off--Reorganization 350 * Temporary layoff 360 Laid-off--End of temporary or seasonal employment 361 Laid-off--End of temporary or seasonal employment--Automatic termination 370 * Elects layoff rather than accept transfer to another position 380 * End of work assignment 390 * Position outsourced
- Death
400 Death 410 Death in the line of duty
- Non-Reappointment
500 Not recommended for reappointment
- Retirement
600 Retirement with pension 640 Retirement without pension 690 Disability retirement 695 Retirement in lieu of layoff
- Student Termination
700 End of student employment (Codes 205 thru 275 have priority.) 701 End of student employment--Automatic termination
* Additional written explanation will be required.
Health Science Center: uthsc.edu/policies/w932_document_list.php?app=HR Space Institute: personnel.utsi.edu/procedures/index.html Institute of Agriculture: ag.tennessee.edu/Pages/UTIApolicies.aspx
- Resignation


text:
Men's Golf
Mark Simpson Invitational
Mon., Sep 26
All day
All day
Erie, CO
Colorado National Golf Club
Colorado National Golf Club
2700 Vista Pkwy
Erie, CO 80516
Watch Info
Not Available
Not Available
Not Available on App
Not Available on App
Not Available on App
More: Mark Simpson Invitational - Men's Golf
Saturday's Play at Pac-12 Championships Cancelled
Pac-12 Men's Golf Championship competition on Saturday has been cancelled due to overnight snow at Boulder Country Club. There will be an attempt to complete the remainder of Friday's second round, along with the entire third round on Sunday.
Wunderli Records Second Hole-In-One of the Season at Pac-12 Championships
Sophomore Nathan Wunderli recorded another hole-in-one and the Utah men's golf team managed to complete its first two rounds at the Pac-12 Championships that are being held at Boulder Country Club.
Golf Heads to Pac-12 Championships in Boulder
The Utah men's golf team head to Boulder, Colo., to compete in the 2017 Pac-12 Men's Golf Championships, which will be held at Boulder Country Club. Action will get underway on Thursday, April 28, and will conclude on Saturday, April 30.
Ninth Place Finish at Hawkeye Invite Closes Out Regular Season
The Utah men's golf team closed out the 2016-17 regular season with a ninth-place finish at the Hawkeye Invitational that was being held at Finkbine Golf Course. The Utes combined to card a three-round total of 17-over par (293-290-298=881) on the weekend.
Hicks and Costello Each Record Hole-In-Ones at Hawkeye Invitational
The Utah men's golf team is currently in a tie for eighth-place following a round and half of play at the Hawkeye Invitational that is being held at Finkbine Golf Course.
Golf Closes Out Regular Season at Hawkeye Invitational
The Utah men's golf team will close out the 2016-17 regular season this weekend, participating in the Hawkeye Invitational. The two-day, 54-hole event will run this Saturday and Sunday, April 15-16, at Finkbine Golf Course in Iowa City, Iowa.


text:
Enjoying a little bite to eat or mini meal should be really easy, but it is one of the hardest things for me. When I get hungry, it's easy to just grab whatever I can find. However, I find that if I can keep my snacking in check, then everything else falls into place.
These Healthy Chicken Salad Bites are a big help. Not only are they high in protein and big on taste (they taste like chicken salad in one yummy little bite), but they are also a perfect make-ahead, grab-and-go snack. So, they're a total win-win. They're also great for meal prep because they keep well in the fridge for 2-3 days.
Healthy Chicken Salad Bites
- 1 cup fresh spinach leaves
- 2 cups cooked and shredded boneless, skinless chicken breast
- 4 ounces Greek yogurt cream cheese slightly softened*
- 2 teaspoons chia seeds
- 1/2 teaspoon fresh lemon zest
- 1/4 teaspoon Italian seasoning
- Kosher salt and black pepper
Heat about 2 cups of water in a large, microwave-safe bowl for 2 minutes and 30 seconds, or until hot and steaming.
Carefully remove water, and place spinach leaves in hot water for 1 minute.
Remove spinach leaves, and squeeze dry.
Finely chop spinach and chicken. Set aside.
In a separate medium bow, beat cream cheese, chia seeds, lemon zest, and Italian seasoning together.
Stir in chicken and spinach.
Season with salt and pepper to taste.
Using a tablespoon, scoop out a scant spoonful of chicken mixture, and shape into a ball.
Repeat with remaining chicken mixture.
Store covered in the fridge for up to two days.
Recipe Notes
*If you can't find Greek yogurt cream cheese, substitute 1/3 less fat cream cheese.
Adapted from Power Snacks.


text:
"Patient care on the ward"
Posted by J.C. (as ),
Approximately Nov 2003 my husband had a knee operation which resulted with him spending time in recovery on the ward. Prior to the op. he was treated very well. He was fully informed of the after care he would receive whilst in recovery on the ward and what he was expected to do to help himself. Everything went well during the operation and he awoke on the ward as he had expected.
It was late evening when he woke up from his op., he was shown his call button and shown how to use his morphine pump (he was to administer this himself when needed).
I visited him the next morning, as soon as permitted. I found my husband writhing in pain and his bed soaked in perspiration. His call alarm was sounding in the corridor just outside the ward and his morphine pump was also bleeping a loud alarm sound.
He appealed to me for help and explained that he had been up all through the night in agony with both alarm noises going off causing disturbance to others on the ward. He went on to say that no-one had seen him, not only through the night, but also that morning.
I searched for a nurse. This took some time, I also felt that I was being a nuisance but was driven by my husbands' distress. Eventually a very kind nurse responded (fresh on the shift) and when told his story, took pity on him, bypassed the morphine machine and gave him an injection. She did not seem happy and sympathised with his distress. My husband quickly fell asleep and was able to rest and catch up on his missed sleep. I returned to work.
On my return to the ward later the same day, I found not only my husband, but also the other men on the ward in need of relief. (They all needed a toilet facility but were unable to move from their beds.) Most had pressed their call buttons with no response for some considerable time, (again the sound of call alarms going off in the corridor just outside the ward). I was compelled to search for staff but without luck. This time I came to a room with urine jars on the side. I took these and distributed them around the ward much to the relief of the men and my husband. I did not realise that this would turn out to be a regular event, that was to result in all of the ward looking forward to my visits.
On closer inspection of my husband, I noticed blood on his sheets. He explained that when he was woken up by his increasing pain later that morning, he managed to persuade a nurse that his morphine machine was not working. They had taken his morphine drip out, passing it across his body, pouring his blood along the way across his chest and bedding and transferred it to his other arm. They made no efforts to clear this trail of blood.
In short, my husband was left in this bedding for close to a week. They eventually gave him a machine that worked. I ended up swapping his sheets around him transferring top to bottom and vice versa just to help freshen him up and remove the 'crime scene', or should I say 'grime scene'. I washed him and refreshed him taking him drinks and toileting bottles as often as I could, not forgetting to assist others on the same ward.
This experience distressed my husband and me. I found some Bank Staff did not understand much of what I was saying but chose to ignore all of us. I also felt on most occasions that some of these staff did not care what was being said, because they would walk off shrugging their shoulders and not return or respond. Nurses were often not in sight and difficult to find. Alarms were on most of the time and unanswered. I was almost in denial with this whilst visiting, believing it was only temporary. In hind sight we have often reflected and realised the horror of this story. What happened to safety, dignity and respect? What happened to common sense?


text:
More on Ziva's Season 11 NCIS Exit07/31/2013
NCIS: Scoop on Cote de Pablo/Ziva's exit from the show and more on season 11 from TVLine's Michael Ausiello
Here's some scoop on NCIS from this week's (Posted on 7/30/13) Ask Ausiello column.
Question: Any news on a replacement for Ziva on NCIS? —Cathy
Ausiello: Yep, and pretty big news at that. As exec producer Gary Glasberg revealed to Matt Mitovich Monday night, it's going to be "a little while" before a full-time agent is brought in to fill the void left by Cote de Pablo. But in the meantime, the show — taking a page from Bones' squintern playbook — will "rotate some fun people" through the agency's doors. "The first two episodes are all about Ziva's departure," Glasberg notes. "And then in the third episode we introduce, for instance, a woman in her 50s who is a few days away from retirement and just needs to fill the desk time. She, in theory, knew Gibbs all the way back to the days of Mike Franks. So we're going to bring in people like that and have some fun with different characters. And then, hopefully, when people are comfortable enough, one will walk in and be The One."
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Looks like Woodview Apartment Homes is no longer available on Rent.com which means this information is likely out of date.
Make sure to check out these similar properties in the area.
Discover a wonderful apartment community which features all of the comforts of home. Woodview Apartments, complete with one and two bedroom floor plans is a must see! Woodview is located in a quiet, serene, convenient, residential neighborhood. Each apartment includes a full size washer and dryer, a wood burning fireplace, quality appliances and all of the conveniences of modern apartment living. Surrounded by majestic forested hillsides, Woodview Apartment Homes are close to a variety of shopping and dining areas. Downtown Beaverton and Portland are just minutes away. For the relaxing lifestyle you have been searching for, look no further than Woodview Apartment Homes.
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120 units
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text:
Calvin Klein
Calvin Klein On My Corner Saffiano Crossbody
Ships from USA , delivers within 14-21 DaysAdd to wishlist
- 13"W x 8"H x 2-1/2"D
- Interior features lining 1 slip pocket and 1 zip pocket
- 7"L double handles; 19"L to 23-1/2"L adjustable and removable crossbody strap
- Zip closure
- Exterior features colorblocking 1 back magnetic-snap pocket and logo
- Gold-tone or silver-tone hardware; varies by color
- Bag converts from crossbody to tote by removing strap
- Silhouette is based off 5'9" model
- Leather
- Imported
- Web ID: 828956607
Special Offers
Return Policy
No questions asked return or exchange*: items may be returned or exchanged for a full refund in the original form of payment or a Vogily Credit within 14 days after shipping. Your satisfaction is our biggest prize, so we do everything to ensure that you are happy with your purchase. All products are 100% authentic, procured from brands directly and are backed by our purchase protection with 10 times money back guarantee. *Please refer to the detailed return policy on the site for exceptions
Ships from USA , delivers within 14-21 Days


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Home > Product Categories > Pro-Audio > Live Sound > Power Amplifiers > ST-PA18
Item #: ST-PA18 MFG #: ST-PA18
List Price:$172.51Our Price:$121.95Quantity Pricing
+ Add to Wishlist + Add to Quote
Required Accessories
RDL PS-24AS 500mA AC/DC Power Supply For Stick-Ons & Rack Ups
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8sp. Oak Finish Studio Rack
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The ST-PA18 features a balanced line level input that may be connected unbalanced. The gain control range will accommodate standard unbalanced levels as well as professional balanced levels. The module bridges the input signal. LOOP OUT terminals permit a balanced input to be fed to additional amplifier modules making the ST-PA18 an ideal component in distributed audio system design. The LOOP OUT may also be used to feed a subwoofer amplifier (see RDL ST-CX2S Subwoofer Filter).
The ST-PA18 output will drive an 8 Ohm speaker or multiple speakers connected to present an 8 Ohm load to the amplifier and it is capable of driving 4 Ohm loads. A red COMP LED is provided to indicate the threshold of the integral compressor. Audio levels that could cause the amplified output to clip are compressed according to two dynamic time constants. Normal audio level signals remain unaffected by the compressor thereby preserving audio dynamics and preventing the compressor from increasing feedback potential when the amplifier is used for paging. The compressor is designed to remain aurally transparent while maintaining clean, unclipped amplified audio for input overloads of up to 20 dB.
The ST-PA18 produces average audio levels and audio clarity normally expected of amplifiers delivering much higher output power. The ST-PA18 operates from an external 24 VDC 1A power supply, sold separately. A POWER LED illuminates when the module is powered. The module provides thermal and output short-circuit protection.
Required Power Supply RDL PS24V Sold Separately
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Monstar Premium Oxygen-Free Bulk Speaker Cable - 16 Gauge
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RDL DRA-35S STICK-ON DIN Rail Adapter - 1 Module
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RDL DRA-35S6 STICK-ON DIN Rail Adapter - 6 Modules
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text:
"Excellent teamwork"
About: Hammersmith Hospital Hammersmith Hospital London W12 0HS
Posted by Anonymous
Having had unsuccessful surgery at another NHS Trust 18 months ago and not reassured with that hospital's follow-up diagnosis and proposals, my partner specifically asked her GP for a referral to a named Endocrinologist and a surgeon at the Hammersmith. We have since been able to thank both gentleman personally for what they and their respective teams have achieved following the excision of an offending tumour on 6 March 2014. What we were not aware of at the time of asking for a second opinion referral was the excellent support that would also be provided through the expertise of the staff in the Imaging Department. From first reception in May 2013 to eventual surgical discharge on 25 March 2014 I really can't see how any of Hammersmith's services could have been bettered. All staff were so very considerate and helpful which provided an air of confidence and reassurance. Our 6-hour round journeys to attend the dozen or so different consultations in the intervening months were well worth it. A sincere thank you all, from my partner and me.
Response from Hammersmith Hospital 3 years ago
Imperial College Healthcare NHS Trust is delighted to receive your review. Thank you for taking the time to express your kind appreciation for the care you received. Your comments are important to us and will be passed on. We hope you are making good process and extend out good wishes for the future.
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text: Sorting type: Most visited Most visited Alphabetical | Images of Chapter 3 Media in category "Category:Chapter 3 Images" Taurus Summoned.jpg Posted in: Chapter 3 Cover 3.jpg Posted in: Chapter Covers Dramatic Entrance.jpg Posted in: Chapter 3 My Udder.jpg Posted in: Episode 2 Taurus KO'ed.jpg Posted in: Chapter 3 Taurus Saving everyone.jpg Posted in: Chapter 3 Retrieved from "http://fairytail.wikia.com/wiki/Category:Chapter_3_Images?oldid=113755" Ad blocker interference detected! Wikia is a free-to-use site that makes money from advertising. We have a modified experience for viewers using ad blockers Wikia is not accessible if you've made further modifications. Remove the custom ad blocker rule(s) and the page will load as expected. Categories: Images by Chapter Add category Cancel Save