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Viruses 2012, 4(12), 3812-3830; doi:10.3390/v4123812
Abstract: West Nile virus (WNV) continues to cause outbreaks of severe neuroinvasive disease in humans and other vertebrate animals in the United States, Europe, and other regions of the world. This review discusses our understanding of the interactions between virus and host that occur in the central nervous system (CNS), the outcome of which can be protection, viral pathogenesis, or immunopathogenesis. We will focus on defining the current state of knowledge of WNV entry, tropism, and host immune response in the CNS, all of which affect the balance between injury and successful clearance.
1. Introduction
West Nile virus (WNV) is a mosquito borne, neurotropic, positive-stranded, enveloped RNA virus in the Flaviviridae family. WNV is related genetically to other viruses that cause severe visceral and central nervous system (CNS) diseases in humans including dengue (DENV), yellow fever (YFV), Japanese encephalitis (JEV), and tick-borne encephalitis (TBEV) viruses. WNV is maintained in an enzootic cycle between mosquitoes and birds, but also infects and causes disease in vertebrate animals including horses and humans. WNV is transmitted primarily by Culex species mosquitoes and the virus amplifies in bird reservoirs, with humans and horses largely considered as dead-end hosts [1]. Although human cases occur primarily after mosquito inoculation, infection after blood transfusion, organ transplantation, and intrauterine transmission has been reported [1]. At present, there are no vaccines or therapeutic agents approved for humans against WNV.
WNV was first isolated in 1937 in Uganda from a woman with an undiagnosed febrile illness [2], and historically, has caused outbreaks of a relatively mild febrile illness in regions of Africa, the Middle East, Asia, and Australia [3]. In the 1990's, the epidemiology of infection changed. New outbreaks in Eastern Europe were associated with higher rates of severe neurological disease [4]. In 1999, WNV entered North America, and caused seven human fatalities in the New York City area as well as a large number of avian and equine deaths. Since then, it has spread to all 48 of the lower continental United States as well as to parts of Canada, Mexico, the Caribbean, and South America. While the majority of human infections are asymptomatic, WNV can cause a severe febrile illness and neuroinvasive syndrome characterized by meningitis, encephalitis, and/or acute flaccid paralysis [5,6,7]. Persistent movement disorders, cognitive dysfunction, and long-term disability all occur after West Nile neuroinvasive disease. West Nile poliomyelitis-like disease results in limb weakness or paralysis. Patients show markedly decreased motor responses in the paretic limbs, preserved sensory responses, and widespread asymmetric muscle denervation without evidence of demyelination or myopathy [8]. Thus, the neurological and functional disability associated with WNV infection represents a considerable source of morbidity in surviving patients long after the acute illness [9,10,11,12,13]. In the United States alone between 1999 and 2012, ~36,000 cases and ~1,500 deaths have been confirmed.
The risk of severe WNV infection in humans is greatest in the elderly and immunocompromised [14,15]. Two studies have estimated a 20-fold increased risk of neuroinvasive disease and death in those over 50 years of age [14,16]. Beyond age, a limited number of host genetic factors have been linked with susceptibility to WNV infection. A deficiency of the chemokine receptor CCR5 increases the risk of symptomatic WNV infection, as a higher incidence (4.2%) of loss-of-function CCR5Δ32 homozygotes was observed in symptomatic WNV infection cohorts compared to that in the general population (1.0%) [17]. A nonsense mutation in the gene encoding 2'-5'-oligoadenylate synthetase/L1 (OAS) isoform is associated with WNV susceptibility in laboratory mice [18]. Correspondingly, a hypomorphic allele of the human ortholog OAS1 is associated with both symptomatic and asymptomatic WNV infection [19]. Finally, an association of single nucleotide polymorphisms (SNP) between symptomatic and asymptomatic WNV infections and IRF3 and Mx1 innate immune response and effector genes has been reported [20]; thus, genetic variation in the interferon (IFN) response pathway appears to correlate with the risk of symptomatic WNV infection in humans. In this review, we will summarize our understanding of the host-virus interface in the CNS and how this determines WNV disease pathogenesis and clinical outcome.
2. Virology and Pathogenesis
Although cellular receptors have not yet been identified definitively, studies suggest that WNV enters cells by endocytosis and fusion with the early endosome [21,22]. Following fusion between the viral and endosomal membranes, the nucleocapsid is released into the cytoplasm and 11 kilobase viral genomic RNA associates with endoplasmic reticulum (ER) membranes. The single open reading frame is translated into a polyprotein and enzymatically processed into three structural proteins (capsid (C), pre-membrane (prM)/membrane (M), and envelope (E)) and seven non-structural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B, and NS5). Negative strand viral RNA then is synthesized and serves as a template for positive strand RNA synthesis [23]. Positive strand RNA is packaged in progeny virions, which bud into the ER to form enveloped immature virions. A maturation step, cleavage of the prM protein to the membrane M protein, occurs in the trans Golgi network by furin-like proteases [24,25,26] and results in a reorganization of E proteins on the virus surface into a homodimeric array [27]; these virions are secreted into the extracellular space by exocytosis.
Following mosquito inoculation into the skin, it is believed that WNV replicates within epidermal keratinocytes and Langerhans cells [28,29]. Migratory Langerhans dendritic cells enter afferent lymphatics and travel to draining lymph nodes [28]. Here, infection and the risk of dissemination are countered by the rapid development of an early immune response including type I and II IFN production and the effector functions of innate immune cells (γδ cells, NK cells, neutrophils, macrophages, and IgM-secreting B cells) [30,31,32,33,34]. Virus produced in the lymph node can enter circulation via the efferent lymphatic system and thoracic duct, and viremia allows spread to secondary lymphoid and visceral organs including the spleen and kidney [35,36]. In peripheral tissues, infection is restricted by innate and adaptive immune responses including serum IgM [37], IFN-α/β [38], IFN-γ [32,39], cytolytic CD8+ T cells [39,40,41], and cell-intrinsic IRF-3-dependent [30,42] antiviral responses.
3. WNV-Induced Pathology in the CNS
WNV causes encephalitis in several vertebrate species by virtue of its ability to infect and injure neurons through direct (viral-induced) and indirect (immune response induced or bystander) mechanisms [43]. Pathologic observations in humans are limited by the small number of autopsy studies on individuals succumbing to WNV infection. In these few reports, gross macroscopic examination of the brain and spinal cord did not reveal any overt pathology [5]. Microscopic examination of the brain in humans and other animals reveals histological changes that are consistent with the clinical disease [5,36]. This includes neuronal cell death, activation of resident microglia and infiltrating macrophages, perivascular and parenchymal accumulation of CD4+ and CD8+ T cells and CD138+ plasma cells, and formation of microglial nodules. These lesions, which can be patchy in distribution, occur in the brainstem, cerebral cortex, the hippocampus, thalamus, and cerebellum [5]. Cellular infiltrates in the meninges also can be present. In some cases, destruction of vascular structures with focal hemorrhage occurs, suggestive of a vasculitis; this may be associated with local compromise of the blood-brain barrier (BBB) [44,45]. Immunohistochemical analysis confirms that WNV antigen is present primarily in neurons from multiple regions of the brain, although other cells (e.g., CD11b+ myeloid cells and possibly astrocytes) may be infected but to lesser degrees [46,47]. In the spinal cord, an intense inflammatory infiltrate around large and small blood vessels is observed with large numbers of microglia in the ventral horn. Anterior horn motor neurons are targeted by WNV [8,48], and studies suggest that axonal transport from peripheral neurons can mediate WNV entry into the spinal cord and induce acute flaccid paralysis [49]. Studies in hamsters reveal that limb paralysis and tremors are directly associated with infection and injury of anterior horn motor neurons in the lumbar section of the spinal cord [50].
4. Neuroinvasion
To establish infection in neurons of the brain, WNV first must cross the BBB (Figure 1). The BBB is composed of endothelial cells, astrocyte foot processes, and pericytes (PCs) and impedes the entry of macromolecules and pathogens from the blood into the brain. The tight junctions between endothelial cells form a diffusion barrier and pose obstacles for pathogens to enter the brain and to infect vulnerable and largely non-renewable neurons [51]. The mechanism by which WNV and other encephalitic flaviviruses cross the BBB remains uncertain. Crossing of the BBB likely occurs through a hematogenous route, as high levels of viremia correlate with greater and more rapid WNV entry into the CNS [52,53]. Intravascular levels of pro-inflammatory cytokines, which are produced during peripheral immune responses, also may modulate WNV entry into the CNS. WNV infection in peripheral tissues induces Toll-like receptor (TLR)-3-mediated secretion of pro-inflammatory cytokines, including IL-6 and TNF-α [44]. Secreted TNF-α can modulate BBB permeability by altering endothelial cell tight junctions, which may allow WNV to cross the BBB and infect neurons [44,54,55]. Semaphorin 7A upregulation after WNV infection also is linked to increased TNF-α production. Mice lacking Semaphorin 7A showed reduced TNF-α levels in serum, less BBB permeability, and reduced viral entry into the brain. [56]. Activation of matrix metalloproteinases also may enhance the flux of WNV by degrading the extracellular matrix of the BBB [57]. In BBB model studies in vitro, treatment with inhibitors of matrix metalloproteinases prevented the disruption of tight junction integrity associated with WNV infection [58].
Beyond compromise of the BBB, in some cases, WNV may penetrate into the CNS through additional mechanisms. Peripheral neurons are susceptible to infection by WNV [59,60]; retrograde axonal transport can bring WNV into the CNS, where transneuronal spread can occur. In contrast to some viruses (e.g., rabies [61]), neuron-to-neuron spread of WNV requires axonal release of viral particles [49]. Other possible entry mechanisms for WNV include (i) infection or passive transport through choroid plexus epithelial cells [62], (ii) a "Trojan horse" mechanism in which the virus is transported by infected immune cells (e.g., neutrophils [34] or CD4+ or CD8+ T cells [63]) that cross the BBB [64], (iii) infection of olfactory neurons and rostral spread from the olfactory bulb [65], or (iv) direct infection of brain microvascular endothelial cells [66]. The precise mechanism of WNV entry into the CNS in humans requires further study, and may differ depending on the route of infection and the pathogenicity of the WNV strain [67].
5. Neuronal Injury
WNV infection of neurons can result in caspase 3-dependent apoptosis, which likely contributes to CNS dysfunction and pathogenesis of severe disease. While no significant difference in peripheral or CNS tissue viral burden was observed in WNV-infected caspase 3−/− mice, these animals were more resistant to lethal WNV infection due to reduced neuronal cell death in the cerebral cortex, brain stem, and cerebellum [68]. Consistent with this, ectopic expression of WNV NS2B-NS3 non-structural proteins activates caspase 3 and induces apoptosis in neuroblastoma cell lines [69], and primary neurons and neuroblastoma cells undergo apoptosis after WNV infection [48,68,70]. Cellular stress pathways including cAMP response element-binding transcription factor homologous protein (CHOP)-dependent apoptotic pathway also likely contribute to WNV-induced neuronal damage [71]. WNV infection may trigger apoptosis by activating non-caspase proteases, such as calpains and cathepsins [72,73]. Finally, WNV infection can induce non-apoptotic pathways of cell death. Cell necrosis can occur, as characterized by extensive cell swelling and loss of membrane integrity likely due to the extensive budding of WNV progeny virions into the ER [74].
In addition to injury imposed directly by WNV infection, neurons may undergo cell death or injury due to bystander damage caused by cytotoxic factors released by neuronal and non-neuronal cells. Neurons that are dying secondary to viral infection or immune-targeted death may release inflammatory molecules (e.g., Cxcl10 L-1β, IL-6, IL-8, and TNF-α) [75,76] with potentially toxic effects on uninfected neurons resulting in irreversible neuronal loss and atrophy. Analogously, glial cells, which are not primary targets of direct WNV infection, can become activated and release excitotoxic amino acids (e.g., glutamic and aspartic acids) and pro-inflammatory cytokines that contribute to the pathogenesis of neurological diseases by virus infections [77,78]. For example, TNF-α and IL1-β released by activated glial cells have direct roles in promoting bystander damage to neurons [79]. Elevated reactive oxygen species secreted by infected or activated microglial cells also may result in oxidative damage to neurons [80].
6. CNS Immune Responses to WNV
Upon entry in the CNS, WNV spreads rapidly between different subtypes of neurons in distinct regions [81]. As neurons are largely non-renewable, controlled immune responses must limit spread and eliminate virus while minimizing neuronal damage [82]. A delay or absence of such responses in genetically deficient mice or immunosuppressed humans results in rapid dissemination, neuronal injury, with an increased risk of mortality. Recent work in animal models has shown that both innate and cellular immune response in the CNS orchestrate control of WNV spread, which ultimately limits the number of neurons targeted for infection or the amount of virus any given infected neurons will produce.
6.1. CNS Innate Immunity
Nucleic acid intermediates of RNA virus replication are recognized by pathogen recognition receptors (PRR) such as TLR and RIG-I like receptors (RLR), which promote an antiviral state by activating IRF-3 and IRF-7-mediated transcriptional programs and type I IFN responses. The importance of these pathways for controlling WNV infection is highlighted by studies in mice that are genetically deficient for key components in this pathway: Type I IFN receptor-knockout mice (Ifnar−/−), Ifnb−/−, Mavs−/−, Tlr3−/−, Tlr7−/−, and Myd88−/− mice all show enhanced viral replication in the CNS and mortality after WNV infection [38,47,83,84,85]. Irf3−/− neurons showed reduced induction of antiviral defense genes including Rig-I, Mda5, and Ifit1, as well as blunted IFNα/β production [42]. In Irf7−/− neurons, IFN-α production was blunted, which resulted in increased WNV infection [86]. Together, these studies suggest that IRF-3 and IRF-7-dependent transcriptional programs are crucial for protective IFN response in neurons. Stat1-dependent signaling pathways in part, determine the susceptibility of specific neuronal subtypes to WNV infection in the brain. IFN-α/β and Stat1-dependent transcription of IFN-stimulated genes (ISGs) inhibited WNV replication in neurons in vitro and in vivo. Rsad2 (also known as viperin), PKR, and RNase L are induced in neurons of the CNS and restrict WNV infection in vivo [87,88].
6.2. Inflammatory Responses
Neurons in the CNS are immunologically active and initiate inflammatory responses by producing chemokines that recruit immune cells (Figure 2). Infection of neurons by WNV induces expression of the T cell chemoattractant Cxcl10, which promotes trafficking of WNV-specific CD8+ T cells via binding to its cognate receptor Cxcr3 [89,90]. Enhanced expression of Ccl3 (MIP-1α), Ccl4 (MIP-1β), Ccl5 (RANTES) by WNV infection leads to Ccr5-dependent trafficking of CD4+ and CD8+ T cells, NK cells, and macrophages. Deletion or truncation of Ccr5 in mice leads to enhanced viral burden and increased mortality [91,92], and appears to be associated with more severe disease in humans [17]. Trafficking of monocytes into the brain, as precursors of macrophages and possibly microglia, can contribute to CNS injury [93] or survival after WNV infection [94], depending on the virulence of the infecting WNV strain. In mice, deletion of Ccr2, a chemokine receptor on inflammatory monocytes, leads to increased mortality after infection by virulent North American WNV strains, and this is associated with reduced monocyte accumulation in the brain [94]. Study with Il22−/− mice demonstrate that reduced levels of Cxcr2, a chemokine receptor mediating neutrophil migration, correlate with decreased viral loads in the CNS [95], suggesting that entry of WNV-infected neutrophils may contribute to pathogenesis. In Tlr7−/− mice, CD45+ leukocytes and CD11b+ macrophages failed to home to WNV-infected neurons due to blunted IL-23 responses, suggesting Tlr7 reduces WNV infection in part, by enhancing IL-23-dependent immune cell infiltration and homing into the brain [85].
6.3. Cellular Immunity
Studies in mice suggest that T cell-mediated immunity is an essential aspect of immune mediated protection from virulent strains of WNV. The lack of a functional CD4+ and CD8+ T cell response results in inefficient clearance of WNV infection from neurons of the brain [39,40,96]. Nonetheless, an over-exuberant CD8+ T cell-mediated response can lead to injury and or death of infected or uninfected neurons. In mice, within a few days of CNS infection, inflammatory cytokines and chemokines produced by resident cells of the CNS attract antigen-specific CD8+ T cells into the CNS [40,89]. In addition, CD40-CD40L and TNFα-TNFα-receptor interactions promote CD8+ T cell migration across brain microvascular endothelial cells, likely by increasing expression of adhesion molecules and modulating the integrity of tight junctions [97,98].
CD8+ T cells control WNV infection in the CNS via multiple mechanisms (Figure 3) including the production of antiviral cytokines (e.g., IFN-γ) or by triggering cell death of target cells through perforin, Fas-Fas ligand, or TRAIL-dependent pathways. Infected neurons up-regulate MHC class I molecules and thus, can be targeted by cytotoxic T cells [99]. Perforin−/− mice showed higher viral burden in CNS and increased mortality after WNV infection [39], as well as a failure to clear WNV resulting in persistent CNS infection. Perforin-mediated control of infected neurons occurs through the granzyme-dependent granule exocytosis pathway, which results in apoptosis of infected neurons in vitro and in vivo [100,101,102]. Fas ligand (FasL) deficient mice also showed increased susceptibility to lethal WNV infection [103]. Interactions between Fas on infected neurons and FasL on CD8+ T cells leads to programmed cell death of neurons through the activation of a death domain and a caspase apoptosis cascade [102,104,105]. CD8+ T cells also use tumor necrosis factor-related apoptosis-inducing ligand (TRAIL; also known as CD253) to restrict WNV pathogenesis by controlling infection in neurons. TRAIL binding to the death receptor DR5 on neurons activates a caspase-dependent apoptosis cascade [41]. Consistent with results establishing a protective effect of effector CD8+ T cells in mice, humans with impaired T cell immunity have a greater risk of CNS infection with WNV [106].
Although T cell responses are important for viral clearance, they can cause irrevocable damage to the host. Under certain conditions, infection of mice lacking CD8+ T cells with an attenuated lineage 2 WNV (Sarafend) strain resulted in decreased morbidity and mortality compared to wild type mice [107]. Consistent with this, depletion of CD8+ T cells in mice infected with an attenuated genetic variant of a North American WNV strain resulted in prolonged survival [108]. Thus, depending on the virological and immunological context, CD8+ T cells either can protect against or contribute to WNV neurological disease.
7. Viral Persistence in the CNS
Although still controversial, persistent WNV infection and inflammation in the CNS of vertebrate animals has been reported in mice, monkeys, and hamsters [109,110,111,112,113]. These results are consistent with earlier studies in animals and humans showing flavivirus persistence after infection with Saint Louis encephalitis, tick-borne encephalitis, and louping ill viruses [114,115,116,117]. In monkeys, the duration of WNV persistence was at least 5.5 months, with infectious virus isolated from the cerebellum and cerebral subcortical ganglia. Virus recovered more than two months after initial infection from these monkeys retained neurovirulence [111]. In hamsters, WNV persistence has been described up to 86 days after initial infection, and this was associated with long term neurological sequelae [112,113]. In mice, infectious WNV was detected in the brains up to 4 months in 12% of mice and viral RNA persisted up to 6 months after infection [110]. Consistent with this, virus-specific B and T cell immune responses persisted in the brains of mice for at least 4 months after infection [109]. Although viral persistence in the CNS has not been documented in humans, chronic WNV infection in the kidney has been reported in some patient cohorts [118,119].
8. Summary and Future Perspectives
WNV continues to spread and cause neurological disease and thus, remains a public health concern in the United States and other countries. Research into the viral and host factors that determine the pathogenesis and outcome of WNV infection is crucial for development of new therapeutic and vaccines strategies. A more complete understanding of the mechanisms of immunopathogenesis in the CNS could facilitate the development tailored anti-inflammatory agents that minimize neuronal damage without preventing clearance. As examples, treatment with the Cxcr4 antagonist AMD3100 enhanced CD8+ T cell trafficking into the parenchyma of CNS and improved survival after WNV encephalitis [120], whereas blockade of migration of nitric oxide-producing inflammatory macrophage using anti-very late antigen (VLA)-4 integrin antibody prolonged survival after WNV encephalitis [121]. Combining such types of immunomodulatory agents with small molecule or antibody-based antiviral molecules [122] that target viral replication or tropism might be a way to maximize viral clearance and minimize neuropathogenesis after WNV infection.
Conflict of Interest
H. Cho declares no conflict of interest. M. Diamond is a consultant for MacroGenics and Elan Pharmaceuticals.
NIH grants U54 AI081680 (Pacific Northwest Regional Center of Excellence for Biodefense and Emerging Infectious Diseases Research), U19 AI083019, and R01 AI074973 supported this work.
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© 2012 by the authors; licensee MDPI, Basel, Switzerland. This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).


text: Hey guys, I was chatting up a buddy of mine and he told me that you guys were a cool site. I really like all of these ideas you guys have on making cash through the internet. Residual income is the way to go! I am excited to be here, and look forward to the future with you all. Peace be unto you! -mick

subset: commoncrawl


text:
Do you ever go through times when you fear your motivation is gone, never to return again? That's how I'm feeling right now. Not about exercise — I'm still going strong there — but more about everything else: school, cleaning, cooking, fixing myself up in the morning, etc…
Although I feel burnt-out to a crisp, I have felt this way before. At the end of every semester, actually. So although I may not feel this way, I know the key is to have faith in myself — faith that my motivation and zest will return when the time is right. I will decompress over break, and I will be ready to start again. And hey, I have some exciting things to look forward to:
(1) I get to start fresh in a new apartment in 9 days, and it is a wonderful place
(2) This semester is over in 8 days
(3) Christmas break is 3 weeks long
(4) Not only do I get to start a new semester in 1 month, but I actually get to start the nursing program
All will be well.
In other news, today is the two-year anniversary of marrying my husband at the courthouse (we later had a big wedding in June, but we did this so that I could move out of the dorms and live together). I am very blessed to be married to my first love and best friend.
For exercise, I did an hour of chest & back weights and 50 minutes of cardio on the elliptical and stationary bike. I tell ya what, it felt GOOD to lug some iron around after doing cardio-only for the last two days! For the next few weeks until we get settled in at our new place, I will keep my workout log brief, but will hopefully get back to sharing it at length when things calm down.
Until next time, keep calm and train hard!


text:
7 Marvel Comic Events That Could Make Incredible Movies
First Civil War, then Age Of Apocalypse, what's next?
First Civil War, then Age Of Apocalypse, what's next?
The company-wide event comic is a staple of Marvel. It can be used to clean the slate, tell a massive story, and do things that the individual comics cannot. These crossovers have represented some of the high and low points for the brand and while comic book fans have always been used to them, movie viewers are just starting to get a taste. Unsurprisingly, film executives have realized that even more so than individual comic arcs, event comics can make for great cinematic inspiration.
Their typically epic scale lends itself well to blockbuster filmmaking and with a few tweaks, it seems that any number of comic book events could make for good films. This year alone will see adaptations of two Marvel classics: Civil War and Age Of Apocalypse. Beyond that, its likely that Infinity War will draw heavily from The Infinity Gauntlet down the road. In terms of the state of the studios that could adapt these stories, Marvel is an established brand and can afford to take more risks with its characters as it begins to phase out old leads in favour of new faces. Fox is in a similar position as it looks to pass the torch from one generation of X-Men to the next.
Regardless of the studio making the adaptation, theyre all pulling from the same library, one which is crowded with crossovers, some good and some bad. Ignoring the filler, these are the arcs that Marvel, Fox, and Sony need to focus on adapting.
Connor loves movies, comics, and TV, and is trying to write for people who feel the same way. When he's not sitting on the couch with his laptop, you might find him lying in his bed with his laptop.See more from Connor


text:
amate i vostri amici, amore la tua musica, amore la tua vita
Hey man, I love your blog! I found lots of new stuff, rediscovered old and found stuff I was looking for ages! I follow you on tumblr so it would be great if you could put an ASK option because I'd like to talk to you about are common musical interests. Mine is Selfdefetingprophecy. Cheers!


text:
Here Is My Story When I Started The Ear Ringing Treatment
Just to let you all know I did get the remedy my buddy was spouting off about, and in the following couple of weeks I could be certain to let you all know if it decreases my ear ringing or not. Try the Tinnitus Cure Programme I Got And you will get all of the details within my own tinnitus miracle review. So while I wait for the 'magic' to kick in, I would have liked to bring up another subject that's extraordinarily near and dear to my heart :
Why Isn't There Enough 'Public Awareness' Being Made For This Evil Afflication?
I mean is it just me, or does this world not consider tinnitus a deserving infirmity to warrant exhaustive media attention and medical research? It appears that in all my years of surring from the annoying ringing, I have almost never seen a single medical or public service commercial looking for aid ( or merely better public awareness ) of this sanity-trying condition. Know what else is crazy? Tinnitus is among the most typical illnesses in the world. I mean heck, just about everyone is affected with a tad bit of ear ringing from time to time? I personally know over five good friends who all have real tinnitus.
Yet we are compelled to suffer silently. With small to no recognition from the world and the medical community of the profound hell we must go thru on a day-to-day basis. Now, glaringly I'm sure that there now isn't any proved 'cure' for this condition, and that naturally the giant pharma only wants to go where the cash is but for God's sake! Isn't there at least some well off tinnitus sufferers who can jump forward for us all and begin to get the wheels of the medical research and discovery machine turning?
It appears ludacris to me that we reside in a world in which we may be able to create vaccines against almost everything yet we can't find some way to get our damaged ears to stop ringing. Anyhow, enough ranting for the moment. I am going to hope and prey That these '3-little-steps' I just took will finish up saving with Tinnitus Miracle.
Talk shortly.


text:
By Poyi (Natalie) Leung
Chief Executive Fernando Chui Sai On denied yesterday that the government lacks a long-term public housing policy, stressing that 6,000 more units will be constructed after 2012 but refused some lawmaker's requests to increase the number to 40,000.
The Chief Executive attended the three-hour plenary meeting at the Legislative Assembly to answer questions from 23 lawmakers concerning a variety of topics from public housing, education, public administration and Macau's development, to environmental protection, labour affairs and support to small and medium enterprises.
One of the most popular topics was the progress of the 19,000 public housing units the government promised to build by the end of 2012 and whether or not the applications for social and affordable housing would be reopened this year.
The top official reiterated the government's continuous efforts to strive to complete the task before the due date, adding that the construction of the 19,000 units should all begin by September this year.
He also disclosed that the government plans to build an additional 6,000 public housing units after 2012, of which 3,500 are in the planning stage and land has been reserved for another 2,500.
He pointed out that in the future, social housing will consist of a bigger portion of the city's public housing, whilst affordable housing will become secondary.
As of the end of 2010, there were 30,890 households living in government-owned properties, the head of the government said.
As the deliberation concerning the draft law on affordable housing was recently completed to be presented for final reading at the legislature today, Chui Sai On promised that once the law is approved, the allocation of the new affordable housing complex in Rua da Tranquilidade do Hipodrómo, Iao Hon, will begin as soon as possible for eligible residents on the waiting list.
Lawmaker Ng Kuok Cheong questioned whether the Chief Executive could make a promise to build 40,000 public housing units and introduce a three-year waiting period for eligible applicants.
However, Chui said he would be "very worried" if the government were to increase the target to 40,000, adding that households on the current waiting lists had already waited a considerable time and promised to give them priority to move into the 19,000 units.
Balance interests
The Chief Executive also said it is "not practical" to make a commitment right now to construct a large number of affordable housing units, as "the government has to balance the interests of residents with private properties".
He explained that there is "interaction between the affordable housing and private property markets", and therefore the government needs to take into consideration "the health of the overall real estate sector in order to prevent the interests of locals with private properties from being affected by "any fluctuation in the market".
Yet the Chief Executive did not comment on when public housing applications may open again, which lawmaker Au Kam San believed would allow the government to understand the demand and ensure better planning in the future.
Meanwhile, Chui Sai On said he had received the petition letter signed by 10 residents on Wednesday who demanded the resumption of their eligibility for social housing applications.
He pointed out that after discussing with Secretary for Transport and Public Works Lau Si Io yesterday, it has been agreed that the government would review the 10 cases "one by one" and attend to them as soon as possible "according to the laws and the actual situation".
Risk assessments
In response to the recent historic downgrade of the United States credit rating and the possible subsequent impact to the global economy, Chief Executive Chui Sai On assured that "Macau's economic foundation is strong enough to resist external fluctuations".
He also said a majority of local assets are in Hong Kong dollars and therefore it remains a "relatively better choice" to peg the pataca to the Hong Kong currency.
Thanks to the booming tourism and gaming industries, the back-up from the Mainland's positive economic prospects as well as the 12th five-year plan, the Chief Executive predicted that there will be favourable conditions to support the territory's future development and also provide opportunities for regional cooperation.
Nevertheless, despite an optimistic forecast of Macau's overall performance in 2011, he stressed that the government will be aware of any instability in the external economy as well as carry out regular risk assessments and be well prepared for the implementation of the fiscal reserve system next year.
Asked by lawmaker Tsui Wai Kwan about the launch of livelihood measures, the Chief Executive said he anticipated the city may report an inflation rate of over 5 percent for the whole year of 2011.
He vowed that the government will closely monitor the trend of soaring price levels during the year especially the impacts on the disadvantaged group.
If inflation continues to worsen, he added that measures to aid the 5,300 underprivileged households will be launched and the function of food banks will also be strengthened. The plan to rein in inflation will cost the government MOP 10 billion, he said.
On the other hand, the Chief Executive said the SAR Government has commissioned the Chinese Academy of Social Sciences, the Institute for Tourism Studies and the Policy Research Centre to examine plans for Macau to become a world travel and leisure hub.
He said Macau needs to step up efforts to diversify the source of visitors, admitting that it is a "hard process" that requires cooperation from the government and society.
Nevertheless, despite continued development in the city, Chui pledged that the government would not fail its commitments to protect the landscape at world heritage sites and the buffer zones, pointing out that the cultural heritage protection law is expected to be submitted to the legislature for discussion "very soon".
Population research
The Chief Executive told lawmakers that the Policy Research Centre will launch a consultation for the 2011-2020 population policy research, which is aimed to investigate the status of the city's overall population, immigration policy and imported labour management.
Moreover, he said the government has the responsibility to ensure the sustainability of the Social Security Fund (FSS), adding that a new actuarial report is being prepared and the 2012 Policy Address will detail the increase in the employer's and employee's contributions to the fund.
On the other hand, he admitted that the government is going to examine whether there is a duplication of functions within public departments and also look into training for senior officials.


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My friend Wendy sent me this very funny clip. What would happen if Facebook was actually played out in real life?
Hello, I'm Annie, an American living in Australia. Writer, researcher, professor, mum. Enthusiast: developmental psych, innovation, ideas, travel, design, stories, and a good laugh.
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A few posts to get you started:
Passing the bridge of sighs
A modest proposal
A modest proposal ii
Adeste fideles
Uncurbed enthusiasm
Liner notes to growing up
Sunday dinner @ 135
Playing big
In praise of late bloomers
Bless her heart
Paging EB White
Nine and a half
Madeleine, 16
Keystone parents
She holds these truths
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Waag Society and Adam Zaretsky's series of workshops and lectures are back in Amsterdam and this time the focus will be biology and bacterial transformation
The second edition of Biorama was a workshop and symposium (set inside a cave) that explored the biology of the underground through the notion of umwelt developed by biologist Jakob von Uexküll and its influence on the development of biosemiotics by Thomas Sebeok.
Second day of the blogathon in Los Angeles. I've lost my notes and my memory is not that great. Still, here's for you a couple of architecture wonders, a strange floating landscape that makes pollution glow, and a project to turn America into a commune
Highlights of Day one includes postborder city, gardening instead of mowing the lawn, temperature architecture, adventures in Kazakhstan and live interviews. Do not forget to bring on the blankets tonight. It's freezing up there on the roof top
Join us in Los Angeles for a series of discussions, interviews, slideshows, panels, talks, and presentations about architecture, landscape, urbanism, art and space
The Game is Up! chose a challenging theme: today's ecological and economical crisis. The festival could hardly ignore that it was stepping on trodden tracks. Yet, the event's pleasant mix of low tech, no-tech and high-tech installations, performances, graffiti, workshops and debates managed to amaze and inspire
Live music and cinema shows, performances, talks, exhibitions, films, workshops, etc. I've got 5 day tickets for April 8th – 13th for you. Anyone interested, just send me your name and email address


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Blogger Comments: Local Losers
Sheriff Ana Franklin. Corrupt to the core. Certain that U.S. Senator Luther Strange would be around to cover her butt during her reign of terror. Told employees in open staff call she would never go to jail in Alabama.
Steven Ziaja and Bones Wilson both cohorts in crime with Sheriff Ana Franklin. Both heavily involved in the Title Mart scheme with Sheriff Ana Franklin. Bones Wilson investor in the Title Marts. Received over $107,000.00 in overtime pay alone. Steven Ziaja loved and lost, and lost, and lost. Thank you, Ana Franklin.
Blake Robinson threatened to take on the FBI on the Sheriff's Office front steps. Member and investor in the Title Mart schemes. Detailed cars at the Title Marts for Steven Ziaja during his normal shift with the Morgan County Sheriff's Office. Transported money for Steven Ziaja from Title Mart dealerships while on duty at the MCSO.
So much changed in Alabama politics in the last week. The king is dead, long live the queen, and all that.
Some – such as former Gov. Doctor Dr. Robert Bentley -- lost everything. Others – like his good-humored but indignant former scheduling director Linda Adams – have forever made an imprint on Alabama history.
These are the winners and losers of the era known as "The Robert Bentley scandal."
John Archibald | firstname.lastname@example.com
John Archibald | email@example.com
John Archibald | email@example.com
John Archibald | firstname.lastname@example.com


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We wanted to give the sofas away instead of dumping them, so I called up the Persatuan Amal Seri Sinar, a charity organisation....the one that provides the large metal donation bins in housing areas for people to donate their clothes, toys, recyclables, etc. They will send a truck to collect furniture and large electrical appliances.
Hmm...it seems like a good way to keep the kids from watching too much TV, though!
They came on Monday and took away my sofa set. The problem is that my new sofa set can only be delivered on Friday, the earliest...which means that we have no sofa to sit on when we watch TV...much to the dismay of our kids.
We only have these 2 little stools we bought from IKEA....it was quite comical to see the kids perched on them...not a very comfortable way to watch TV!
Hmm...it seems like a good way to keep the kids from watching too much TV, though!


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With National Butchers' Week coming up at the end of the month (24th-30th March), it is a pleasure for me to be working on this fascinating guide to the craft of butchery to be published by Chelsea Green on the 27th. In fact the book explains the whole journey that our meat makes, from farm to table, and is a bit of an eye-opener for anyone who cares about how their meat is sourced.
In The Gourmet Butcher's Guide to Meat master butcher Cole Ward aims to revive the traditional culinary art of butchery – an often overlooked but vitally important aspect of the farm-to-table movement.
The most comprehensive guide available to the complete process of meat production, the book will be invaluable to small-scale butchers, to chefs who want to broaden their skills, to farmers and smallholders, to the many who attend butchery courses, and to anyone who cares about how their meat is sourced.
The book features two master British butchers: Balson Bros, Bridport, Dorset – Britain's oldest family butcher (as featured in BBCTV's Hidden Histories series), and MacDonald Bros, Pitlochry, Scotland, owned and run by the MacDonald family since 1928.
"A good butcher is an ethical professional who knows the provenance of his or her meats," Ward writes. "I want to give everyone an understanding and appreciation of my craft and its culinary artists, and I want to celebrate and support struggling small farmers and quality-meat producers. So my mission is nothing less than to bring back culinary butchery—a craft that we must never lose."
A major benefit of the book is the enclosed CD that contains over 800 step-by-step photos demonstrating how to cut up a side of beef, a side of pork, a whole lamb and a chicken.
Cole Ward is a master butcher based in Vermont, USA, who combines hands-on butchery with teaching his craft at culinary academies, colleges and agricultural and sustainable-living conferences.
Karen Coshof is a photographer and film producer specializing in environmental subjects.
National Butchers' Week UK: 24th-30th March 2014
The Gourmet Butcher's Guide to Meat by Cole Ward and Karen Coshof is published by Chelsea Green, RRP £35.99 including CD with 800 images, and is available through all good high street and online booksellers.


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- November 18, 1915 - June 8, 2017
- La Porte, Indiana
of Glen's Passing
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Glen was born on November 18, 1915 and passed away on Thursday, June 8, 2017.
Glen was a resident of La Porte, Indiana at the time of passing.
Interment will follow at the Patton Cemetery, LaPorte, Indiana where he will receive full military honors.
Memorial contributions may be made to the Honor Flight of Chicago, 938 W. Montana Street, Chicago, IL.


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|LUMINOUS SUNSET by Sea Dean
6" x 8" on Windpower
To view my Gallery or purchase this painting please visit Daily Paintworks. Larger paintings in the same series available by contacting me.
Although I generally celebrate Famous Masters that have passed away, I am honouring Robert Genn's birthday today because he is such an inspiration to Canadian artists. When I researched this blog, I found his Sunset on Cortez, which, reminds of my own LUMINOUS SUNSET above.
Robert Genn was born in Victoria on May 15th 1936. He currently has terminal cancer and is resting at his home in British Columbia. Having lost several family members to Cancer, including my father, my heart goes out to Robert and his family at this difficult time.
When he can, Robert still takes time to write a blog, as in the precis of Abraham Maslow's work below.
1. Systematically study, understand and neutralize the effects of lower needs.
2. Accept the world in all of its complexity, mystery and ambiguity.
3. Take cues from the winners in this world, not the losers.
4. Keep the company of the doers, not the talkers.
5. Play your personal game on as many levels as you're able.
6. Fall in love with your processes, innovations, dreams and higher ideals.
7. Be sensitive to and welcome the arrival of peak experiences.
8. Have no guilt when you see yourself becoming compulsive and proactive.
9. Allow yourself to be swept up in your personal "must."
"Where was the human potential lost? How was it crippled? A good question might be not why do people create, but why do people not create?" (Abraham Maslow, 1908-1970)
"In my experience, artists with highly developed self-critical faculties are often referred to as "talented." Robert Genn
Cat # 13162 Luminous Sunset


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Your business vehicles don't need to be exposed to so much risk if you make the proper regulations when you or your employees drive.
It does not matter whether you only use your personal car to attend meetings down the street or you own an entire flock of vehicles that travel the country to deliver your goods or services, you need to purchase commercial auto insurance in order for your business vehicles to be covered. But commercial auto insurance can only do so much, and so you'll need to take extra steps to really protect your vehicles. Here are a few business-vehicle regulations to enact to reduce the risk to your business vehicles.
Driving Rules
- Mandatory Seat Belt Use – Nearly every state has enacted some sort of seat belt law. The reason being seat belts help prevent deaths and limit the extent of injuries in vehicle accidents.
- Absolutely No Cellphones – Distracted driving is the leading cause of motor accidents on the road, and cellphone use is even illegal in most states. Prohibit your employees from texting or calling while they are behind the wheel.
Vehicle Use
- Limit Personal Use of Business Vehicles – Some employees may use their personal car for business, too, which makes this one a bit difficult. You should limit your business vehicles for strictly work purposes only.
- Lock Vehicles at All Times – In order to decrease the risk of theft, employees should lock the vehicles at all times, no matter how short of time the employee will be away from the car. When possible, the car should be parked in a secure and well-lit area.
These tips along with a comprehensive commercial auto insurance policy can keep you covered. For policies across the globe, contact the independent insurance professionals at Lloyd S. Berkett Insurance Agency in Los Angeles.


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Two is an excellent age in so many ways. It's also the age when you want to ship your children off to distant planets because they are so incredibly maddening. But it's also really, really excellent.
One of my favorite things about hanging out with Addie right now is the adventure she is having with language. Being two allows one a delightful level of creativity with proncunciation, meaning, and logic without self-consciousness; this makes communicating with Addie particularly exciting. For example, she's been singing this version of "Twinkle, twinkle" lately, which she made up all by herself:
Twinkle, twinkle, little moon
How I wonder why you spoon
Up above the world so high
Like a giant pizza pie
Twinkle, twinkle, little moon
How I hope to see you soon.
Cool, huh? Brilliant little genius, she is. She also says things with such a sweet little lisp--a bird's nest is a bird's "nesthsh" and so on. So, this is all endearing and wonderful. When it's not particularly frustrating, that is.
We're doing a lot of talking about emotions lately. I was getting fed up with Addie's pretty much constant tantrums a while back, and when I get frustrated, I read. A discussion of parenting books on my favorite-ever parenting website, Parenthacks, led me to a 1961 book by Haim Ginott called Between Parent and Child. It's written in this old-fashioned, Cold-War-civil-defense-manual tone and there's a whole lot of sexist stuff about what mommies and daddies do and don't do, but if you can get past that, I think it offers some pretty good advice. For example, it recommends offering simple, clear answers to kid's complex questions (I know, duh, but for some reason I had gotten into the habit of giving Addie some long-winded answers lately, and this was a good reminder to shut up a liitle).
Ginott's book also reminded me to simply acknowledge Addie's feelings as they were happening rather than try to fix them, interrogate them, or teach her to suppress them. For example, these are the types of conversations we were often having, typically precipitated by my asking her not to do something such as, oh, I don't know, sticking peas in her nostrils:
A (lower lip protruding prominently): Mommy, I'm sad!
M: Why are you sad, Addie?
A (now kicking and screaming, peas flying everywhere): Because I am!
Nowhere to go from there, right? I mean, how do you explain the problems with circular logic to a toddler? So now I'm trying something that looks like this:
A: Mommy, I'm sad!
M: It's okay to feel sad, Addie. We all feel sad sometimes and it's good to express it. But peas should usually go in our mouths, sweetie, not in our noses.
A (lip still protruding but no kicking and screaming): Okay, mommy. Mommy? I can't breathe!
M: I know, my darling girl. Let's get those dang peas out of your nose.
Not exactly Jedi magic, but the whole "It's alright to cry" thing seems to really work with her. This makes a lot of sense to me. In fact, my therapist really helped me to feel my feelings, too, to the tune of a couple hundred bucks a month. But it worked--I don't stick peas up my nose anymore, and I know it's okay to feel a liitle sad about it. Whatever--the idea is that you teach your children to identify and express their emotions in appropriate ways. Pretty healthy stuff.
The other Ginott gem that Eric and I have been using with Addie for a while is the old giving lots of choices trick. The key is to make sure you provide manageable and acceptable choices. In other words, the choices have to be simple enough to not overwhelm a two-year-old, and also contain alternatives that are acceptable to you as a parent.
For instance, asking a toddler what she wants for dinner is a bad idea (she might say "marshmallows" or "bats' eyes," neither of which is on the menu around here). Asking her if she wants a hot dog or a quesadilla is a better alternative--at my house, anyway. At your house, feeding your kid a hot dog might be as bad as the bats' eyes. The point is that you provide a range of appropriate choices for you.
This is particularly useful when you get the ubiquitous "no" response. Addie won't even hear your question before her ruby-red lips are forming the word "no," so we've had to develop some creative strategies around this. Of course she doesn't want to change her pull-up! She likes lugging around three pounds of pee-soaked cotton between her legs! But the choice she has is not really whether the pull-up is going to be changed. It has to be. Her choice is whether she wants it changed in the living room or in the dining room, or whether she wants to do it herself or with my help. Acceptable choices.
Ginnott also talks about why bribing and threatening are bad, though those habits have been a little harder for us to break. Still, we're working on it. And his strategies are certainly making my life with Addie more excellent than frustrating.


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12/6/10: Comment left on my blog post about coming out to my older teenage daughter.
"What you just went through - coming out to your wife and to your daughter, but mostly coming out to yourself and becoming okay with the fact you're gay - should be met with the utmost level of self-respect, love and acceptance you can muster for yourself.
"You've spent years and untold energy on trying to be someone else because of what you believed was the right course of action for you. And you learned, regardless of how hard you try, you are the man you were created to be and that man insists on being acknowledged and loved. He deserves to be happy, to feel transcendent love and to have a life that's integrated, not compartmentalized; that's actualized, not just pining away in another situation, wishing it were different ...
"My ex-wife and I were married 19 years ... When we decided to separate, it was after a conversation that should've ended the marriage five years earlier, but "for the kids' sake" we hung in there, only to find our friendship disintegrate and a horrible "DADT" [Don't Ask, Don't Tell] policy implemented. Staying together after that conversation became really toxic for us. Thank heavens for a therapist who walked me through my "next steps" and helped me understand that the most loving, compassionate course of action was to divorce.
"I can tell you that giving up my marriage and, quite honestly, leaving Mormonism took a lot of thought and courage, and not without some sense of loss, too.
"The life I live now is so much better and infinitely more honest and happier than what I had before. There isn't a day when I don't think how glad I am I made this decision and that I would never, ever go back to hiding, attending a church that doesn't allow me to be open about who I am and that I now have a church where I am not only accepted, but loved for exactly who I am."
(I began the process of coming out in October 2010. I'm working on writing a memoir about the year following that coming out, and in order to help me stay on task, I've decided to publish this ongoing series of posts based primarily on the blog - entitled "Invictus Pilgrim" - that I kept during that year.)


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Cereal Leaf Beetle Phenology
The Cereal Leaf Beetle growth stage model is a heat-unit or growing degree-day (GDD) model in which the pest's growth and development is based on the pests's physiological response to temperature.
The growth stages are defined according to ranges of accumulated GDDs as follows:
Cereal Leaf Beetle Phenology References
Harcourt, D. G., J. C. Guppy, and C. R. Ellis. 1977. ESTABLISHMENT AND SPREAD OF TETRASTICHUS-JULIS (HYMENOPTERA - EULOPHIDAE), A PARASITOID OF CEREAL LEAF BEETLE IN ONTARIO. Can. Entomol. 109:473-476.
Blodgett, S., C. I. Tharp, and K. Kephart. 2004. Cereal leaf beetle (Insects and Pests B-21) Montana State University Extension Service, Bozeman, MT.
Winter Wheat Phenology
The Winter wheat growth stage model is a heat-unit or growing degree-day (GDD) model in which wheat's growth and development is based on the plant's
physiological response to temperature, photoperiodism, and vernalization.
The growth stages are defined according to ranges of accumulated GDDs as follows:
Winter Wheat Phenology References
Klepper, B., R.W. Rickman, J.F. Zuzel, and S.E. Waldman. 1988. Use of growing degree days to project sample dates for ceral crops. Agron. J. 80: 850–852.
Miller, P., W. Lanier, and S. Brandt. 2001. Using Growing Degree Days to Predict Plant Stages, Montana State University Extension Services, MT200103.
Rickman, R., S. Waldman, and B. Klepper. 1995. PLANTEMP 2.11. EM 8308. Oregon State Univ. Ext. Servide (August).
Thomason, W.E., M.M. Alley, S.B. Phillips, and D.J. Parrish. 2009. Using the Virginia Cooperative Extension Climate Analysis Web Tool to Better Manage and Predict Wheat Development. Virgina Coop. Extenstion, Publcation424-004
Wysocki, D., and M. Corp. USING SEED SIZE, PLANTING DATE, AND EXPECTED YIELD TO ADJUST DRYLAND WINTER WHEAT SEEDING RATES. Oregon State University Extension. Accessed October 2014: http://extension.oregonstate.edu/catalog/html/sr/sr1068-e/014.pdf
Cook, James R. and Roger J. Veseth. Wheat Health Management. APS Press, 1991. p. 10-15
Downy Brome Phenology
Downyh Brome(aka Cheat Grass) is an annual bunchgrass, usually germinating in the autumn, overwintering as a seedling, then flowering in the spring or early summer.
The growth stages are defined according to ranges of accumulated GDDs as follows:
Downy Brome Phenology References
Ball, D.A., B. Klepper, and D.J. Rydrych. 1995. Comparative Above-Ground Development Rates for Several Annual Grass Weeds and Cereal Grains. Weed Sci. 43(3): 410–416.
Nesse, P.E., and D.A. Ball. 1994. Downy Brome, PNW 474. (October).
Enter Life Form
Select the life form of interest from the dropdown. If you have a custom life form, enter a name and a temperature threshold for dormancy.
Enter Custom Life FormIf you have a custom life form, enter a name and a temperature threshold (degree Celcius) for dormancy.
Enter DatesIf you have a custom life form, enter a name and a temperature threshold (degree Celcius) for dormancy. Select the start and end dates for the calculation of the accumulated growing degree days.
Get Map of GDDClick on the 'GET GDD' button.
A visual of the accumulated growing degree days for your species will be overlaid on the map. A title and a colorbar are present to aid interpretation of the map.
Add LayersYou can add layers (such as state boundaries) to the map by clicking on the 'Layers' button on the map.
Get GDD at Point LocationsYou can get specific GDD values and life cycle information at point locations on the map by clicking on the 'GetValues' button on the map. A window will pop up on the map. You can move the marker to the desired location or enter the latitude/longitude coordinates of your location. You can modify the date for the current GDD. Click the 'Current GDD' button.
Katherine Hegewisch
Postdoctoral Fellow
University of Idaho, Moscow
khegewisch [at] uidaho.edu
Donovan VanSant
Graduate Student
University of Idaho, Moscow
vans1746 [at] vandals.uidaho.edu
Erich Seamon
Data Manager
University of Idaho
Sanford Eigenbrode
REACCH Project Director
University of Idaho
Paul Gessler
Cyber Infrastructure Team Lead
University of Idaho
John Abatzoglou
Associate Professor, Geography
University of Idaho, Moscow
jabatzoglou [at] uidaho.edu


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Rams push Ravens to overtime but fall in Ottawa
OTTAWA – In a back-and-forth game between two top ten matchups, the No. 8 Ryerson Rams fell 71-65 to the No. 4 Carleton Ravens in overtime.
Turnovers were the key issue for both teams, and Ryerson finished the game with 19 while Carleton racked up with 21. The Rams converted on far more, creating 20 of their 65 points off turnovers.
The game was lopsided through the first half, and the first quarter went in favour of the Rams. Finishing on an impressive three-point buzzer beater from Sofia Paska, Ryerson entered the first quarter break up 18-10.
The second quarter was that of the Ravens, behind strong efforts from Jenjen Abella and Catherine Traer. Abella hit a three to open the scoring in the quarter and lead an eventual 7-0 Ravens run, but the Rams maintained the lead until 0:42 remaining when Stephanie Carr hit another three to tie the game at 27. Both teams scored two more points and ended the half 29-29.
The second half was much more even, with the largest lead of the third quarter at six points with 4:13 remaining for the Rams after Cara Tiemens scored on three straight possessions, with two threes and a layup off a steal. The Ravens would not give up and clawed back in, ending the quarter on a left hand layup from Traer to put the score at 49-47 for Ryerson.
In the final and lowest scoring frame of regulation, both teams traded baskets and ended the game 58-58. The score of the fourth quarter was 11-9 for Carleton, with a total of nine players contributing.
Into overtime! Carleton outscored Ryerson 13-7, making the final score 71-65 for the Ravens. All of Ryerson's overtime points came from the free throw line, adding seven to their total of 19 made on the game.
Paska was eight for eight from the charity stripe, totaling 19 points and nine rebounds, narrowly missing another double double. Tiemens was also essential to the Rams, adding three 3-pointers and 16 points. Traer led all scorers with 20, and added eight rebounds, seven steals and five blocks for an impressive evening.
There were a total of 10 lead changes and seven ties throughout the game. Ryerson moves to 13-5 on the season and will face the Ottawa Gee-Gees Saturday night for the second of their back-to-back games and to wrap up the regular season.


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Our little Nate has been a big Alan Jackson fan for about the last eight months. It started off with his love for the song "Goodtime" he then shortly after discovered some of Alan's oldies but goodies. Some of his other favorites are Country Boy, Chattahoochee, Livin on Love, and Summertime Blues. Some other of Nate's favorites include Toby Keith "Me and God Love Her" and Brad Paisley "Start a Band". He has a few alternative/rock songs he likes as well as the beach boys. He will tell you right away when a song comes on if he likes it or not!
For your viewing pleasure...
Wednesday, February 25, 2009
1 comment:
- AnonymousMarch 12, 2009 at 7:47 PM
he is such a little performer!!!! :)ReplyDelete
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Good Afternoon Blogland!!
A Very Happy Easter to You All!!!
So far our Good Friday has been great ... our daughter is 21 today and we have had a fab morning .. and we are all off out tonight for a Chinese in our local restaurant and then the "big party" tomorrow night!!
thought you might like to see two pics
22nd April 1990 ... awh bless!!
19th March 2011... on her engagement
We are just a little bit proud of "our little girl"!!
ANYWAY ... on to the winner of my blog candy
thank you all so much for entering and joining in the celebration
I put you all in random.org
and the winner is ...
Congratulations!!! please email me on email@example.com :)
Have a brilliant Easter whatever you do ... catch up with you all soon


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I guess I should start with Washington. I'm looking at the pictures I took on my phone now, trying to piece it all together. The talks, the meetings, the awesome tour where we learned the origin of words like "lobbying" and why the Washington Monument is in two tones. And how the Blair House came about (it involves Winston Churchill walking around in his nightgown, smoking his awful cigars, and running into the very proper Eleanor Roosevelt in one of his night wanderings).
I arrived in Washington after more than a combined 24 hours of flying. That was still OK. What was not was how long it took, firstly to get to immigration, and secondly, to clear it. Two hours! There were some English girls standing behind me, chatting. They were pretty empty-headed (their talk running to boys and babies, not to mention fashion) so I enjoyed eavesdropping on their conversation.
Then a taxi with a nice Ethiopian driver who took me on the long leisurely ride (the airport was really far from the hotel) and guess what, the customs officers had broken one of my bags although I had used an approved TSA lock. Sharon had warned me that that could happen as it had in her case. But it was still unpleasant. Nothing was taken, however.
When I got to the hotel, I met two of our liaison officers (there were three in all) who would be looking after us for the duration of the three weeks, Norman and Phyllinda (we called her Linda for short). We arrived on a Saturday and had to go look for food on our own.
I discovered a nice fish place at the back of the hotel (it was Lent so I was not eating meat at the time). Or drinking, for that matter.
The next morning we were due to go for a tour of Washington. Our tour "guide" turned out to be a volunteer who was actually working at the Kuwait Embassy (I'm sorry now that I didn't take a picture of her, she was something else!). First stop; the White House. People were standing outside the park and looking across at very fierce female policemen guarding it and keeping people out. Turned out that the Afghan president was paying Obama a visit. It had been even worse when it was Putin. Worse because Obama had not wanted him to visit but Congress had approved it and he had no choice, and also worse because of the security required when that unpopular head of state came a-calling.
But we waited around in the gusty wind, hands in pockets, while our guide (I can't remember her name but although she was an expert on US history and all the little quirks around there, she had a European accent) told us about the origin of Blair House. Seems that Churchill had trouble with insomnia. And he was put in the Rose Room, which a little girl might enjoy but not a man's man who smoke cigars unapologetically (sometimes dear boy, a cigar is just a cigar), polished off his food like a solid trencherman (by contrast, I heard that Hitler was actually a vegetarian). Anyway, he took to pacing up and down the White House corridors in his nightgown, where Eleanor Roosevelt, a very proper lady, encountered him, in his nightgown. Now, this was either in the lead up to WW2 or it was during that conflict. So there was no choice but Churchill would keep visiting). Eleanor convinced her husband to buy Blair House across the street and put that recalcitrant, insomniac Englishman there.
And so, here's a picture of Blair House:
And here's the White House. It is a pretty modest size. Most of the group were surprised at how small it was. In fact, it hadn't become the "white" house until after Teddy Roosevelt who painted it white. At least I think it was Teddy. Am beginning to forget what our guide told us. (This is why these posts should be done immediately and not four weeks later).
After the White House we went to the Willard Intercontinental Washington where the term "lobbyists" comes from. Apparently, Ulysses S. Grant used to flee to the hotel to escape an unpleasant domestic situation which involved his father-in-law, and people got to know about it. So they would come to the hotel in hopes of schmoozing with him in the lobby, trying to gain special favour and turn him to their point of view on something or other. And thus the term "lobbying" was born.
Everyone was especially fascinated by this story. But then, we were fascinated by all her stories.
After that it was a trip to Capitol Hill where she explained how the US government was run. And then to the Lincoln Monumnet where there are many secrets. Like this face at the back of Lincoln's head which is apparently Robert E. Lee, the vanquished foe.
After the tour, I asked to be let off to go see Washington museums. I figured it would be the only day I would get to see the museums (after our meetings for the day it would either be too late or I would be too tired to go, and I was right). Alberto (from Spain) decided to come with me. And that is how I got to know him. We had lunch at a cafe in one the museums and decided to start with the Smithsonian National Museum of the American Indian. It was wonderful, especially the gift shop, where I decided to get a children's book for my friend Katherine's son (I thought it would be way cooler than getting him a generic children's book from someplace else and it was - when she received it she read him the story twice in the 15 minutes and he wanted to know all about the raven and the sun...well, you get the picture)
Here are some shots from the Washington museums:
A rainbow caught unawares...
A prevalent theme:
We also went to the Museum of Air and Space (Alberto wanted to catch the Wrights' exhibit)...and I enjoyed that too...but this was the only picture I took there.
And the Hirshhorn which was full of art exhibits - and we went through the "Days of Endless Time" exhibit which was ethereal to say the least. I didn't take any pictures though, because we were not allowed. Alberto was a little impatient (when they say endless time, they mean endless time)...and then we took a cab back to the hotel (although Alberto would have rather walked and taken in the architecture) because I was way too tired with all the walking.
Washington was where jet lag was at its apex...so a lot of the times, we got back to the hotel and I would intend to take a nap and wake up to find it was the wee hours of the morning.
The meetings were interesting and somewhat contentious. Some of the people on our trip (like Alberto) were actual trade negotiators and would not let something slip past that they thought was erroneous). Others were really sarcastic economists (how come our economists in Malaysia are not like that?).
Anyway, the first five days (we were five days in Washington) went by. And Washington stands out as the only state where I never made it to a bookstore. It didn't matter...New York was next and Emily had sent me a list of bookstores to visit.


text:
Adapt, Adjust, Respond: Perspectives on Current Trends In American Colleges and Universities
Tension over the norms, values, and practices within higher education and between higher education and American culture has been multiplying since World War II. Numerous concepts and theories characterized the range of these forces and factors. This review discusses five such factors that appear to effect change in higher education in the United States. These five trends indicate an increasing frequency of the discussion of and calls for change in higher education in American Colleges and Universities.
American culture; higher education; chnage; values
Higher Education Perspectives. ISSN: 1710-1530


text:
Ever since I moved in about a year ago, my office has been a perpetual work in progress.
It's been a challenge to organize and decorate the space, and to make it more personal without having to spend too much.
Little by little I've been making some progress, with some improvements here and there.
This corner is my latest addition to date :
Just looking at A's collage all framed up like that makes me really happy :).
Coupled with a picture of the fam, a native basket, a matryoshka stuffed toy I got on one of my trips, and a small bunch of fresh baby's breath, I think this corner looks charming and definitely, personal.
Now, on to the next…
Stay tuned!