text:
NeuroView| Volume 64, ISSUE 1, P17-20, October 15, 2009
Viral Infection Leading to Brain Dysfunction: More Prevalent Than Appreciated?
Anthony N. van den Pol
Department of Neurosurgery, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520, USA
Open ArchiveDOI:https://doi.org/10.1016/j.neuron.2009.09.023
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Virus infections of the brain can lead to transient or permanent neurologic or psychiatric dysfunction. Some of the complexities in establishing the causal role of viruses in brain disease are explored here.
For most of the major neurological diseases afflicting us, including Alzheimer's, Parkinson's, multiple sclerosis, narcolepsy, schizophrenia, and others, we do not know the cause. We may know which neurons are involved, for instance that Parkinson's is caused by a loss of substantia nigra dopamine neurons, and narcolepsy is caused by loss of hypothalamic hypocretin neurons, but why these cells are lost remains a mystery.
Viral infections of the brain may result in a clearly diagnosed fulminant encephalitis, sometimes resulting in lethal consequences. However, a growing understanding of the biology of the hundred or so viruses that infect the brain and the resultant host responses, together with improved diagnostic tools and the lessons learned from animal models, have raised the possibility of viral causation of a number of more subtle neurological conditions. Yet in contrast to the acute encephalitic presentation of viral infection of the brain, providing evidence for a causative link between viral infection and chronic neurological dysfunction remains challenging.
Why Are Viral Infections of the Brain So Complex to Understand?
There are a number of underlying reasons. Much of experimental science today is based on testing hypotheses, with the expectation that if the hypothesis is correct, then the outcome is predictable. But even a single type of virus can act in an unpredictable manner in infected individuals, infecting different regions of the brain to evoke different symptoms, or causing CNS disease in only a small minority of infected individuals. Such diversity makes it difficult to provide consistent evidence in favor of viral origin hypotheses.
Robert Koch, who shared the Nobel prize in 1905, the year before the award was bestowed on Cajal and Golgi, was a brilliant German doctor who began his research in his bedroom and studied a number of potentially dangerous bacteria, including anthrax and tuberculosis. At a time when a debate still existed whether microorganisms could cause disease, Koch's seminal experiments led to a substantially clearer appreciation that microorganisms, particularly bacteria, can cause disease. Koch's postulates, the gold standard in establishing the cause of infectious disease, suggest in part that if a microorganism caused a disease, it should be found in every case of the disease, and conversely, that the microorganism should not be found in those not afflicted with that particular disease (
Koch, 1890
Koch, R. (1890) Klassiker der Medizin, Herausgegeben von Karl Sudhof: Die Ätiologie und die Bekämpfung der Tuberkulose. J.A. Barth, Leipzig 1912 edition.
). But it is difficult to identify any virus that infects the CNS to cause brain dysfunction that behaves in a manner fully consistent with Koch's postulates. The virus that comes the closest is rabies, an enveloped RNA virus. But even with rabies, if the virus does not enter the CNS of an infected individual, then no serious symptoms will occur.
A case in point for a well-known neurotrophic virus for which a neurological symptom cannot be predicted is polio virus, a small positive-strand RNA virus. Fewer than one in a hundred nonimmunized people that have a productive infection from polio virus show neurological symptoms. Despite an enormous focus on polio, we still do not understand how and why the polio virus selectively infects the motor system of these unlucky few that show neurological symptoms associated with poliomyelitis. Thanks to a world-wide immunization effort, polio has almost been eradicated, with some pockets remaining in less-affluent countries. Similarly, the unrelated West Nile virus, another RNA virus, also causes serious neurological dysfunction in fewer than one in a hundred people that become infected with the virus from a mosquito infusion. West Nile virus has become a concern in the last ten years after outbreaks were first noted in New York City; the suggested source of the current virus in the USA is from infected wild or captive birds or an infected mosquito, arriving here from Africa or the Middle East. Ironically, West Nile virus was actually imported into New York City about 60 years ago when it was thought that it might serve in an oncolytic capacity, and a number of humans with cancer were purposefully infected with the virus in the hope of attenuating their cancer (
Southam and Moore, 1954
Southam C.M.
Moore A.E.
Am. J. Trop. Med. Hyg. 1954; 3: 19-50
). The virus was not particularly effective in cancer treatment, and its use was discontinued. That only a small number of infected individuals ever show neurological consequences with these two well-studied viruses underlines the difficult task of assigning cause for infections of the brain by the many other less-studied viruses that sporadically infect the CNS.
Infections of the brain are less common than that of other organs and depend on infrequent events that allow the virus to penetrate the blood-brain barrier. Most systemic viruses do not enter the brain. Those that do may take advantage of rare events that include break down of the blood-brain barrier or infection of Trojan horse-like immune cells that are competent to cross the blood-brain barrier but, in doing so, subsequently release viruses within the brain (
van den Pol, 2009
van den Pol A.N.
J. Virol. 2009; 83: 420-427
). The route and site of entry may play a large role in the ultimate symptoms generated. Viruses can cause neurological problems due to a number of mechanisms including lytic effects on brain cells (cytomegalovirus), induced apoptosis (vesicular stomatitis virus, VSV), or secondary damage due to release of glutamate, DNA, and other inducers of further brain damage. Other viruses such as rabies do not kill neurons but instead commandeer cellular transcriptional pathways to express viral rather than neuronal genes; this results in neurons that no longer function as neurons but look normal upon routine pathological examination.
Similar to the real estate adage "location, location, location," the same is important also for viral infections of the brain. Unlike other organs such as liver where the specific location within the liver infected by the virus does not substantively alter the symptoms, the precise region in the brain that is infected plays a key role in the type of resulting dysfunction. Limbic infections will manifest a completely different syndrome than infections of motor or sensory systems. Viruses such as cytomegalovirus, rubella, and lymphocytic choriomeningitis virus cause serious abnormalities if the developing brain is infected, and depending on the site and age of fetal infection, can generate overlapping but distinct symptoms such as deafness, blindness, epilepsy, hydrocephalus, and/or mental retardation in a manner directly related to what part of the brain was infected. The age of the infected individual also plays a large role in some infections; different viruses cause neurologic dysfunction at different stages of life. Some viruses, for instance West Nile virus, are more likely to cause neurological problems in the elderly. Conversely, the DNA virus cytomegalovirus is considered the most common infectious agent causing permanent neurologic dysfunction in the developing human brain but presents little danger to the mature brain. Other viruses including wild-type VSV show an age-dependent shift in the type of neurons infected. These factors all contribute to the difficulty in trying to demonstrate that the cause of an existing neurological syndrome may be viral in origin.
Indirect Effects, Activation of an Immune Response against Infected Cell
Must a single disease be associated with a single microorganism? This perspective may not hold for viral infections of the brain. Take, for example, the case of multiple sclerosis (MS). If MS is due to an autoimmune attack on oligodendrocytes, it might be initiated by a transient viral infection of those cells. While no single virus has consistently been linked with MS (
Atkins et al., 2000
Atkins G.J.
McQuaid S.
Morris-Downes M.M.
Galbraith S.E.
Amor S.
Cosby S.L.
Sheahan B.J.
Rev. Med. Virol. 2000; 10: 291-303
), morbilliviruses such as measles and/or other viruses that sometimes infect oligodendrocytes have been associated with the disease (
Sips et al., 2007
Sips G.J.
Chesik D.
Glazenburg L.
Wilschut J.
De Keyser J.
Wilczak N.
). Viral diseases are particularly difficult to study and interpret in humans. But in animal models of MS, a surprisingly large number of unrelated viruses can induce an MS-like CNS disease. Viruses that can cause MS-like disease, associated with an autoimmune-mediated loss of oligodendrocytes, include measles, VSV, vaccinia, mouse hepatitis, Semliki Forest, Theiler's, Chandipura, and Venezuelan equine encephalitis virus (
Johnson, 1998
Johnson R.T.
Viral Infections of the Nervous System.
Lippincott-Raven, Philadelphia1998
). The animal studies give more credibility to the view that at least in some cases, MS in humans may be initiated by viral infection and argue it is the host immune response to infection that matters for disease progression rather than the specific virus itself. In other cases, such as after lymphocytic choriomeningitis viral infection, damage to neurons may also be due to attack of the infected cells by killer T cells of the systemic immune system.
The immune response to viruses is complex but generally starts with the frontline innate neuronal and glial antiviral defenses including an upregulation of interferon and antiviral downstream genes including OAS/RNaseL, MxA, ISG15, and PKR within hours of an infection (
van den Pol et al., 2007
Robek M.D.
Ghosh P.K.
Ozduman K.
Bandi P.
Whim M.D.
Wollmann G.
); this is followed within days by an upregulation of acquired immunity with an increase in virus-specific B, T, natural killer cells, and macrophage/monocytes. In addition, many viruses, even those with only a handful of genes, have evolved an ability to block or subvert interferon-mediated cellular antiviral defenses. For instance, the M protein of VSV blocks nuclear pores, whereas Sindbis and Venezuelan equine encephalitis virus block interferon responses by attenuating phosphorylation of downstream STAT1 and STAT2 pathways (
Yin et al., 2009
Yin J.
Gardner C.L.
Burke C.W.
Ryman K.D.
Klimstra W.B.
J. Virol. 2009; 83: 10036-10047
). Florey devoted part of his Nobel address for the discovery of penicillin to biological warfare, not the use of biological weapons by humans, but rather the idea that microorganisms are constantly battling one another for survival. In a sense, the struggle between viruses and the cells of the brain can also be viewed as a battlefield, with survival of the cells or virus dependent on complex strategies and counterstrategies that each employs.
Genes and Genetic Variability
A single mutation can dramatically alter a virus's ability to subvert cellular antiviral defenses, as in the case of the M51 mutation in VSV that not only reduces viral infection, but also increases the relative infectivity in cancer cells relative to normal cells (
Stojdl et al., 2003
Stojdl D.F.
Lichty B.D.
tenOever B.R.
Paterson J.M.
Power A.T.
Knowles S.
Marius R.
Reynard J.
Poliquin L.
Atkins H.
Cancer Cell. 2003; 4: 263-275
). Some viruses such as wild-type VSV can mutate quickly and exist in the wild not as a single genome but as a population of closely related genomes, allowing the virus a survival advantage if a particular clone has an increased success rate at infecting particular types of cells, but also adding to the complexity in determining a preferred cellular target in the brain for the virus or for determining if and which virus clone might be responsible for a neurological problem.
From a "host" perspective, our own antiviral defenses are also complex and regulated by a wide variety of genes. Some gene alleles may enhance protection from specific viruses, others may protect from one virus but increase susceptibility to another. Humans with CCR5 delta 32, a mutated chemokine receptor, show a reduced potential for developing AIDS and consequent AIDS-related dementia from human immunodeficiency virus, whereas West Nile virus encephalitis is more common in people with the same mutated receptor (
Glass et al., 2006
Glass W.G.
McDermott D.H.
Lim J.K.
Lekhong S.
Yu S.F.
Frank W.A.
Pape J.
Cheshier R.C.
Murphy P.M.
J. Exp. Med. 2006; 203: 35-40
). Several mutations in the interferon pathway affect the susceptibility for herpes simplex encephalitis; reported mutations altering herpes infections include those affecting UNC-93B, STAT1, and Toll-like receptor 3 (
Arkwright and Abinun, 2008
Arkwright P.D.
Abinun M.
Curr. Opin. Infect. Dis. 2008; 21: 217-222
Sancho-Shimizu et al., 2007
Sancho-Shimizu V.
Zhang S.Y.
Abel L.
Tardieu M.
Rozenberg F.
Jouanguy E.
Casanova J.L.
Curr. Opin. Allergy Clin. Immunol. 2007; 7: 495-505
). We are only beginning to appreciate which genes might modulate viral susceptibility, but genetic differences in individuals undoubtedly contribute to the complexity of CNS responses to viral invasion.
Invisible Attacks and Delayed Actions
A common treatment for a number of psychiatric diseases such as depression or anxiety disorders is the use of serotonin selective reuptake inhibitors (SSRIs) that increase extracellular serotonin. Interestingly, there are viruses that can exert the opposite action and reduce serotonin levels, theoretically having the opposite effect of the SSRIs. Viruses such as wild-type VSV can rapidly and selectively infect and destroy serotonin (and norepinephrine) neurons in young mice and rats. A subsequent immune system-mediated response eliminates all trace of the virus from the brain, leaving a permanent reduction in serotonin neurons with consequent behavioral alterations (
Mohammed et al., 1992
Mohammed A.K.
Maehlen J.
Magnusson O.
Fonnum F.
Kristensson K.
Neurobiol. Aging. 1992; 13: 83-87
) with no viral signature left behind. The neurotransmitter and behavioral changes resulting from this initial infection may last the lifetime of the organism, despite the lack of any trace of the virus in the brain and with little detectable viral-mediated neuropathology evident by standard screening methods at the end of life.
Viral infections can also generate neurological problems years or decades after the initial infection. Chicken pox, actually not a pox virus but a double-strand DNA enveloped herpes virus, can remain latent in neurons for decades, to return years later as shingles when the live virus is regenerated from its latent genome, causing protracted periods of itching or pain. The herpes simplex genome can also remain latent in peripheral neurons for long periods before the active, replication-competent virus is regenerated and travels down the axon to once again infect the periphery. Some viruses leave a latent imprint on the brain that causes neurological dysfunction decades after the virus has been eliminated from the brain by the immune system. Postpolio syndrome is one example. Humans that have had symptoms of poliomyelitis and recovered can again show symptoms, such as weakness of affected limbs, 30–40 years later. In science and medicine, we are accustomed to a cause and effect within a relatively short time span. Consequences of viral infections that occur decades after the primary infection, often in the absence of any trace of a virus, is another serious problem in assigning cause postfacto to viral infections.
Detection, Correlation, and Causation—Borna Disease Virus and Mental Illness
An interesting virus from a psychiatric perspective is Borna disease virus (BDV). BDV is a slowly replicating, enveloped, negative-strand RNA virus that can enter the brain, infect neurons, often in the limbic system, and remain active for long periods in the CNS without generating neuronal lysis. BDV is unique in its mononegavirales order in that it replicates in the cell nucleus; other viruses of the order replicate in the cytoplasm. BDV causes behavioral disturbances in a remarkably wide variety of species, including mouse, rat, llama, ostrich, chicken, horse, cat, fox, dog, and monkey. These disturbances include falling, tremor, abnormal posture, hyperactivity or hypoactivity, increased aggression, and paralysis. In some rodent species, BDV may cause only mild symptoms or may be asymptomatic, whereas in other species such as horse, BDV can cause severe CNS symptoms often leading to death. It is difficult to imagine that a virus that can cause neurological dysfunction in so many species might not also do so in humans. Intriguingly, an increased incidence of BDV has been reported in patients in some psychiatric hospitals, where it has been associated with depression, bipolar disease, or schizophrenia. But a complication of correlating psychiatric disease symptoms with BDV (and other viruses) is that there are no standard tests for the presence of BDV infectivity. Tests widely ranging in sensitivity (including nested and nonnested RT-PCR, immunocytochemistry, and ELISA) have generated quite different sets of data on the relative occurrence and correlation of BDV with different psychiatric syndromes, making a clear determination of causation more difficult and adding fuel to the debate gauging the role of BDV in mental illness (http://www.cdc.gov/ncidod/eid/vol3no2/hatalski.htm). This confusion is further exacerbated by the fact that the diagnostic tests assay only for the presence of the virus in the blood or CSF, a step away from knowing where the virus might be within the brain. Additionally, the presence of BDV in some asymptomatic humans cannot necessarily be used to discount a BDV cause of brain disease, as illustrated by the example of the very small percent of individuals that show neurological symptoms after polio virus infections.
Potential for Use of Viruses to Treat Brain Disease
While the above arguments have highlighted that viruses can be potent adversaries, it is worth noting that some of these same features of viruses can also be harnessed to treat neurological disorders. Viruses are particularly good at bringing their genomes into a variety of cells. Beneficial genes can be engineered into viruses, particularly adenoassociated virus and the lentiviruses. These replication incompetent vectors can infect neurons with minimal complications, and lead to long-lasting transgene expression. Another potential role for viruses is in the treatment of brain cancer. Replication competent viruses such as VSV, myxoma, and herpes are being generated to target, infect, and kill glioblastoma (
Chiocca, 2008
Chiocca E.A.
Curr. Opin. Mol. Ther. 2008; 10: 38-45
). Other viruses such as H1 have been designed to provoke an immune attack on cancer cells (
Raykov et al., 2008
Raykov Z.
Grekova S.
Leuchs B.
Aprahamian M.
Rommelaere J.
Int. J. Cancer. 2008; 122: 2880-2884
In summary, the same mechanisms of infection described above that make it difficult to prove viral causation of brain disease also make it equally difficult to reject viral hypotheses for CNS dysfunction. Viruses probably do constitute an unrecognized direct or indirect cause of a number of neurological syndromes. What percentage of these syndromes is due to viral infections, and what is due to many other potential causes remains to be determined.
I thank G. Wollmann for helpful suggestions. Support provided by NIH AI/NS48854 and CA124737.
DOI: https://doi.org/10.1016/j.neuron.2009.09.023


text:
Is Herbert v. Kitchen Still Good Law?
In his order dissenting from the denial of Alaska's request for a stay, Judge O'Scannlain cited Herbert v. Kitchen (2014).
Is Herbert v. Kitchen still good law? How should we understand it? Is the precedent valid because it is still on the books? Is it invalid because we now know that (at least) 5, and perhaps 6 Justices no longer support that decision to stay the judgment? Is there a difference between Hebert granted a stay in an emergency context, but a stay is not appropriate following the formal certiorari process? Have the circumstances changed to render this precedent obsolete?
On the one hand, nothing the Supreme Court has done would, in the least, cast doubt on that precedent of super-recent vintage. On the other hand, what the Court has *not* done casts serious doubt on this precedent. By denying certiorari on the petition for certiorari from the 10th Circuit, the stay originally granted in Herbert v. Kitchen has been lifted.
I don't think this is a valid citation. And,unless the Court says otherwise, Herbert should not be relied on in this context. Barely a year old, Herbert v. Kitchen (January 6, 2014), has been superseded before it even made it into the U.S. Reports. How often does that happen?

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Bhopal: Madhya Pradesh Home Minister Bhupendra Singh on Thursday said that the five casualties during farmers' agitation in Mandsaur occurred during police firing.
"Five persons were killed in police firing," Singh told PTI over the phone.
The minister's remarks assume significance as the authorities had been claiming that the police had not fired during protests at Pipliamandi in Mandsaur district in which five farmers were killed two days ago.
Minutes after the incident, the then Mandsaur Collector SK Singh had told PTI that the police told him categorically that "neither did they fire nor did they have any orders to fire".
Asked what provoked the police to fire, the home minister said it is being probed in the magisterial inquiry.
However, he said the situation was now peaceful in western Madhya Pradesh.
Meanwhile, contingents of Rapid Action Force (RAF) were deployed on Thursday in Mandsaur which has been on the boil since the violence two days ago.
Two companies of RAF, comprising around 100 men each, have moved into Pipliamandi, the police said.
While two companies of RAF have been posted in the district's Garoth area, another two have been deployed along the Mwoh-Neemuch Highway to prevent any untoward incidents, they said.
The situation is tense but under control, the police said.
DIG Ratlam Range Avinash Sharma is camping in Pipliamandi where farmers, agitating for the last seven days for loan waiver and better crop prices, defied prohibitory orders on Wednesday, beat up officials and policemen and resorted to violence and arson.
Senior police officials have also been deployed to oversee the law and order situation in all sub-divisions of Mandsaur district, the official said.
The situation in western Madhya Pradesh is posing a major challenge for Chief Minister Shivraj Singh Chouhan and providing a rallying point for the opposition parties.
The Shivraj Chouhan government had sought to cool tempers by announcing certain measures, including a loan settlement scheme for those cultivators who had defaulted on repayment of farm loan borrowed by them earlier.
The scheme will cover around six lakh farmers, with accumulated dues of Rs 6,000 crore, according to the government.


The Brazilian Carnival Ball over the years has supported various Brazilian Charities. An article in the 2001 Brazilian Ball magazine, tells the story of these and the impact on the small town which gave birth to the Brazilian Ball.
Created a wing to house the diagnostic clinic.
Purchased a MRI and mammography machine.
Obtained and shipped donations from Wellesley Hospital and Mount Sinai Hospital which included beds, mattresses, bed linens medicine and medical equipment.
Created a working garden where patients are able to pass the time planting vegetables and flowers.
Created a working wing for patients with autism.
Built two wings to allow separation of men and women within the home.
Created a dental clinic for treatment of the residents.
Built a recreation centre for the residents.
Helped in the renovation of St. Judas' Church.
Helped in the renovation of the Igreja da Abadia.
In the city of Batatais, the Brazilian Ball created a pavilion for the APAE Association of Fathers and Friends of exceptional children.


Freedom Point is part of the Sheepshead Mountain Recreation Area which is open for picnics, games, hiking, fishing and enjoying nature. Groups can reserve the pavilion for special events. There is a watchable wildlife nature trail that provides access to Maney Lake, a small lake open to fishing. No boats are allowed on the lake.
Take Interstate 15 north from Butte about 13 miles to the Elk Park exit. Turn right off the ramp and go under overpass to Forest Service road #442 and continue driving for 6 miles. The Sheepshead Recreation Area is on your right. Freedom Point is the first entrance on your right.


text:
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An E-Discovery Renaissance: Finding Your Place at the Table
By Stephanie Maw Booher, Director-E-Discovery Services, Keating Muething & Klekamp
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Overall Landscape
Most of us will agree that the massive growth and sophistication of Big Data, Cloud, Mobile, Networking and related technologies in specifically the last three to five years, have driven what can be perhaps the most clear presentations of cause and effect, yin and yang, and even supply and demand in recent market history. In the world of e-discovery, I see Big Data as the most looming factor driving this change and growth, knowing that in 2011 we learned that Electronically Stored Information ("ESI") was found to be doubling or tripling every two years, with estimates of 1.8 Zettabytes (1.8 trillion GB), where 85 percent of that data lived in private business domains subject to litigation, and hence down-cycle e-discovery preservation, collection, document review (ouch!) and document production costs.
Fast forwarding to 2016: we see the simultaneous forces of expansion and contraction operating within Big Data. On one hand—the continued advancement of mobile, remote, personal data sources and penetration of consumer devices and technologies, all for use in generating business content, plays a known but often ignored or under-diagnosed symptom contributing to this unprecedented proliferation of Big Data. On the other hand, the development and fairly recent sophistication around Big Data mining and analytics technology has worked to reduce and make manageable this otherwise massive and complex e-discovery data playing field. We are somewhat paradoxically therefore simultaneously increasing the volume and complexity of dispute evidentiary data sources and volumes, while later working to decrease and reduce this same volume and complexity to a more manageable and therefore less costly amount as it pertains to the discovery phases of a litigation or regulatory investigation matter.
The development around big data mining and analytics technology has worked to reduce and manage the otherwise massive and complex e-discovery data playing field
The former scenario, combined with the fact that today's workforce is largely mobile and virtual in nature rather than local, physical or hard-wired in nature, makes it very difficult for companies (translation: IT and IS officers and management) to develop, evolve and enforce the inescapable and rightfully top-of-mind cyber-security defenses necessary to protect enterprise, client and partners' data, much less be able to attempt to granularly identify what data exists where within the enterprise, when and where and why is it being modified, transferred and duplicated, both internally and externally. Add to that the pain points surrounding real-time communications technology such as SMS, FaceTime and Skype. While fairly innocuous to enjoy from a personal communications standpoint, they can take on a more ominous tone when facing litigation, regulatory investigations and particularly e-discovery requirements, which, in the United States, require "preservation" and later "collection" and "production" of this Electronically Stored Information ("ESI") and typically in its native file format accompanied by a litigation database loadfile reflecting all of the objective, system and file metadata field values surrounding each and every document record, or in this scenario, message communication item. Sounds easy, right? Eh, not exactly. While mobile device forensics, cell site analysis, and more advanced encryption technologies help the cause, they are still, at least from our experience, typically only partially exhaustive due to the inherent hardware and collection software limitations present, absent, among other things, the ability to leverage an operating system for collection purposes. All of this to say it's one thing to preserve, collect, process/cull, review and produce standard unstructured e-discovery data such as e-mail messages and Word documents, but completely another thing to do the same for text messages, VOIP messages and social media content, for example.
An important discipline known as Records and Information Management, or RIM, has recently received growing interest, attention and service offerings with what I will call a "re-branding" of sorts, as information governance, or IG – and, notably, not just by my fellow technologists within the organization, but by risk, audit, operations and perhaps most notably, business unit and c-suite management. While IG is viewed as imperative by a few, necessary by some, providing a competitive advantage by still some others, it is still largely in its burgeoning phases of development, and, as a result, is often still viewed as an unnecessary financial investment to correct and re-build an often very complex and sometimes outdated set of records management and corporate governance policies, procedures, and even more daunting – advanced technologies – now available to enhance these initiatives.
A Rich Array of Service Offerings
Somewhat predictably, we find this is often the case when it comes to solo entrepreneurs and small to medium sized businesses, but perhaps surprisingly, from the corporate viewpoint as well, where even with compelling business case support, there may still be little internal incentive to pursue these project initiatives, because they require an initial upfront cost expenditure without a guaranteed matching revenue recapture stream in return. The good news is that as critical IT and IS stakeholders, your place at the table has just been set as one of a King's Royal Feast, where as members of the King's court and leaders of the Renaissance, you now have an unprecedented array of e-discovery services and product offerings in the market from which to choose–in-house, on-demand, managed services, and Cloud, or some combination of these services models to provide a custom solution. Taking a nod in part from Right Sourcing strategy, if you find yourself a buyer in this market, you should find e-discovery technology providers more willing than ever before to consider alternative pricing models and negotiate fees and costs.
With e-discovery mergers and acquisitions at an all time high, most providers are working hard to remain autonomous and continue to provide, in particular, their on-demand/per-project e-discovery collection, processing/culling, managed document review and electronic document production services that for many years served as their bread and butter. These services that once earned them a premium profit with multiple non-negotiable fixed price points are now commonly open to à la carte, per phase, flat fee or even fixed bid pricing models. As a result, companies facing these e-discovery hurdles on a more limited basis and therefore less interested in a longer term commitment involved with a managed services or enterprise Cloud services solution, for example, are well advised to negotiate all price points offered and even the pricing structures themselves. Having earned your seat at the table, do not pass up this invitation – enjoy.
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Fire specialists from the Tonto National Forest plan to burn 40 acres of vegetative debris piles on Thursday, March 7. This one-day prescribed fire treatment will occur north of Payson along the south side of the Beaver Valley area.
Fire specialists from the Tonto National Forest plan to burn approximately 75 acres of piles on Tuesday and Wednesday, February 12, and February 13, 2019. The piles are located on national forest near the Vista Verde subdivision from 136th Street to 170th Street, north of Rio Verde/Dynamite Drive.
The thinning of trees throughout the Coconino National Forest has produced piles of branches, which will be burned this week near Flagstaff and in the Stoneman Lake area which will produce smoke visible to surrounding residents and travelers.


Discussion question: Is patriotism a positive sentiment in the world?
My father joined the navy after the Second World War partly out of a sentiment of patriotism.
Bertrand Russell once noted that patriotism is the willingness to kill and be killed for trivial reasons.
George Jean Nathan once suggested that patriotism is often an arbitrary veneration of real estate above principles.
The energy, idealism and unadulterated patriotism in that room was overwhelming.
Protesters may reject patriotism, embracing dissent over displays of American spirit.
patriotism is surely a powerful force, but those emotions can only go that far.
And I think there's an emerging patriotism, decision-makers care more about their country.
Thursday, February 19, 2015 Print Email Respond to editor Teaching a lesson in patriotism..
Tens of millions of netizens contributed to an epic display of collective patriotism.
They sought to frame his choice as evidence of his presumed disloyalty and lack of patriotism.


One dress.. Two ways… It is always fun to style a cloth in different ways and I love doing it. If you guys remember I already wore this skirt / maxi dress when I went to Sikkim, click here to see. Yes ! I wore a maxi dress as a skirt here and a graphic tee over it. I rolled up the sleeves and made a knot at the center. Created fusion look by adding indian beaded necklace and a pair of weaved shoes to make the look more edgy. I really love the color contrast and how the print is gelling together with graphic. What do you guys think about this look??


Our sweet Sterling Silver star and moon Pendant will give any outfit a celestial vibe. Made in .925 silver a crescent moon with a tiny star will add glam to any look. Perfect to layer and an easy way to show off your individuality, from work to weekends. Chain not Included.


The Sacrament of the Anointing of the Sick is a sign of Christ's healing presence in the world. Anyone, regardless of age, whose health is seriously impaired or threatened, may be anointed. Contrary to the experience of many older Catholics, this sacrament is not only for those in immediate danger of death, but for anyone whose illness is more than mild or passing, or whose physical, spiritual or emotional health causes them serious worry or anxiety.
We provide an annual Anointing of the Sick for the homebound and a Communal Anointing on one weekend in the fall at the 5:00PM Liturgy on Saturday, and the 8:30 AM and 11:00 AM Liturgies on Sunday morning. We also have the Anointing of the Sick at St. Vincent's Apartments in the fall.
Contact Sister Eleanor Guerin, RSM, for more information.


text:
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 Playoff and World Series Stats and Results - Baseball-Reference.com
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{{cite web | title = Playoff and World Series Stats and Results - Baseball-Reference.com | url = http://www.baseball-reference.com/postseason/ | date = 2010-01-09 | archiveurl = http://archive.today/Y3yoD | archivedate = 2013-02-25 }}
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You Are Here > Baseball-Reference.com > Playoff and World Series Index
Baseball-Reference Playoff and World Series Index
Search the P.I. Play Index for your own Postseason leaderboards and facts. For example, Every Postseason Walk-Off Hit (1903-2008)
Batting and Pitching Leaders for World Series Career and Single-Series.
Batting and Pitching Leaders for LCS Career and Single-Series.
Batting and Pitching Leaders for Division Series Career and Single-Series.
Batting and Pitching Leaders for Playoffs Career and Single-Year.
Click on a Series Title for game results and series statistics.
Click on a Team for team rosters and statistics.
Series outcomes and season records are in ()'s, and series winners (or leaders for in progress series) are in Bold and listed first.
IE users can mouse over the abbreviated team names to view the team names and records for non-World Series matchups.
World Series - Modern era from 1903 to present (also played as exhibitions from 1884 to 1890)
ALCS - American League Championship Series (first played in 1969)
NLCS - National League Championship Series (first played in 1969)
ALDS - American League Division Series (played in 1981 and after 1994)
NLDS - National League Division Series (played in 1981 and after 1994)
Championship Series - Played by first and second half NL winners in 1892
* - denotes wild card team
2009 World Series (4-2): New York Yankees (103-59, AL) vs. Philadelphia Phillies (93-69, NL)
ALCS (4-2): New York Yankees vs. Los Angeles Angels of Anaheim NLCS (4-1): Philadelphia Phillies vs. Los Angeles Dodgers
ALDS (3-0): NYY vs. MIN ALDS (3-0): LAA vs. BOS* NLDS (3-0): LAD vs. STL NLDS (3-1): PHI vs. COL*
2008 World Series (4-1): Philadelphia Phillies (92-70, NL) vs. Tampa Bay Rays (97-65, AL)
ALCS (4-3): Tampa Bay Rays vs. Boston Red Sox* NLCS (4-1): Philadelphia Phillies vs. Los Angeles Dodgers
ALDS (3-1): BOS* vs. LAA ALDS (3-1): TBR vs. CHW NLDS (3-0): LAD vs. CHC NLDS (3-1): PHI vs. MIL*
2007 World Series (4-0): Boston Red Sox (96-66, AL) vs. Colorado Rockies* (90-73, NL)
ALCS (4-3): Boston Red Sox vs. Cleveland Indians NLCS (4-0): Colorado Rockies* vs. Arizona Diamondbacks
ALDS (3-0): BOS vs. LAA ALDS (3-1): CLE vs. NYY* NLDS (3-0): ARI vs. CHC NLDS (3-0): COL* vs. PHI
2006 World Series (4-1): St. Louis Cardinals (83-78, NL) vs. Detroit Tigers* (95-67, AL)
ALCS (4-0): Detroit Tigers* vs. Oakland Athletics NLCS (4-3): St. Louis Cardinals vs. New York Mets
ALDS (3-1): DET* vs. NYY ALDS (3-0): OAK vs. MIN NLDS (3-0): NYM vs. LAD* NLDS (3-1): STL vs. SDP
2005 World Series (4-0): Chicago White Sox (99-63, AL) vs. Houston Astros* (89-73, NL)
ALCS (4-1): Chicago White Sox vs. Los Angeles Angels of Anaheim NLCS (4-2): Houston Astros* vs. St. Louis Cardinals
ALDS (3-0): CHW vs. BOS* ALDS (3-2): LAA vs. NYY NLDS (3-0): STL vs. SDP NLDS (3-1): HOU* vs. ATL
2004 World Series (4-0): Boston Red Sox* (98-64, AL) vs. St. Louis Cardinals (105-57, NL)
ALCS (4-3): Boston Red Sox* vs. New York Yankees NLCS (4-3): St. Louis Cardinals vs. Houston Astros*
ALDS (3-0): BOS* vs. ANA ALDS (3-1): NYY vs. MIN NLDS (3-1): STL vs. LAD NLDS (3-2): HOU* vs. ATL
2003 World Series (4-2): Florida Marlins* (91-71, NL) vs. New York Yankees (101-61, AL)
ALCS (4-3): New York Yankees vs. Boston Red Sox* NLCS (4-3): Florida Marlins* vs. Chicago Cubs
ALDS (3-1): NYY vs. MIN ALDS (3-2): BOS* vs. OAK NLDS (3-1): FLA* vs. SFG NLDS (3-2): CHC vs. ATL
2002 World Series (4-3): Anaheim Angels* (99-63, AL) vs. San Francisco Giants* (95-66, NL)
ALCS (4-1): Anaheim Angels* vs. Minnesota Twins NLCS (4-1): San Francisco Giants* vs. St. Louis Cardinals
ALDS (3-1): ANA* vs. NYY ALDS (3-2): MIN vs. OAK NLDS (3-2): SFG* vs. ATL NLDS (3-0): STL vs. ARI
2001 World Series (4-3): Arizona Diamondbacks (92-70, NL) vs. New York Yankees (95-65, AL)
ALCS (4-1): New York Yankees vs. Seattle Mariners NLCS (4-1): Arizona Diamondbacks vs. Atlanta Braves
ALDS (3-2): SEA vs. CLE ALDS (3-2): NYY vs. OAK* NLDS (3-0): ATL vs. HOU NLDS (3-2): ARI vs. STL*
2000 World Series (4-1): New York Yankees (87-74, AL) vs. New York Mets* (94-68, NL)
ALCS (4-2): New York Yankees vs. Seattle Mariners* NLCS (4-1): New York Mets* vs. St. Louis Cardinals
ALDS (3-2): NYY vs. OAK ALDS (3-0): SEA* vs. CHW NLDS (3-0): STL vs. ATL NLDS (3-1): NYM* vs. SFG
1999 World Series (4-0): New York Yankees (98-64, AL) vs. Atlanta Braves (103-59, NL)
ALCS (4-1): New York Yankees vs. Boston Red Sox* NLCS (4-2): Atlanta Braves vs. New York Mets*
ALDS (3-2): BOS* vs. CLE ALDS (3-0): NYY vs. TEX NLDS (3-1): ATL vs. HOU NLDS (3-1): NYM* vs. ARI
1998 World Series (4-0): New York Yankees (114-48, AL) vs. San Diego Padres (98-64, NL)
ALCS (4-2): New York Yankees vs. Cleveland Indians NLCS (4-2): San Diego Padres vs. Atlanta Braves
ALDS (3-1): CLE vs. BOS* ALDS (3-0): NYY vs. TEX NLDS (3-0): ATL vs. CHC* NLDS (3-1): SDP vs. HOU
1997 World Series (4-3): Florida Marlins* (92-70, NL) vs. Cleveland Indians (86-75, AL)
ALCS (4-2): Cleveland Indians vs. Baltimore Orioles NLCS (4-2): Florida Marlins* vs. Atlanta Braves
ALDS (3-2): CLE vs. NYY* ALDS (3-1): BAL vs. SEA NLDS (3-0): FLA* vs. SFG NLDS (3-0): ATL vs. HOU
1996 World Series (4-2): New York Yankees (92-70, AL) vs. Atlanta Braves (96-66, NL)
ALCS (4-1): New York Yankees vs. Baltimore Orioles* NLCS (4-3): Atlanta Braves vs. St. Louis Cardinals
ALDS (3-1): BAL* vs. CLE ALDS (3-1): NYY vs. TEX NLDS (3-0): ATL vs. LAD* NLDS (3-0): STL vs. SDP
1995 World Series (4-2): Atlanta Braves (90-54, NL) vs. Cleveland Indians (100-44, AL)
ALCS (4-2): Cleveland Indians vs. Seattle Mariners NLCS (4-0): Atlanta Braves vs. Cincinnati Reds
ALDS (3-0): CLE vs. BOS ALDS (3-2): SEA vs. NYY* NLDS (3-1): ATL vs. COL* NLDS (3-0): CIN vs. LAD
1994 No Postseason played this year.
1993 World Series (4-2): Toronto Blue Jays (95-67, AL) vs. Philadelphia Phillies (97-65, NL)
ALCS (4-2): Toronto Blue Jays vs. Chicago White Sox NLCS (4-2): Philadelphia Phillies vs. Atlanta Braves
1992 World Series (4-2): Toronto Blue Jays (96-66, AL) vs. Atlanta Braves (98-64, NL)
ALCS (4-2): Toronto Blue Jays vs. Oakland Athletics NLCS (4-3): Atlanta Braves vs. Pittsburgh Pirates
1991 World Series (4-3): Minnesota Twins (95-67, AL) vs. Atlanta Braves (94-68, NL)
ALCS (4-1): Minnesota Twins vs. Toronto Blue Jays NLCS (4-3): Atlanta Braves vs. Pittsburgh Pirates
1990 World Series (4-0): Cincinnati Reds (91-71, NL) vs. Oakland Athletics (103-59, AL)
ALCS (4-0): Oakland Athletics vs. Boston Red Sox NLCS (4-2): Cincinnati Reds vs. Pittsburgh Pirates
1989 World Series (4-0): Oakland Athletics (99-63, AL) vs. San Francisco Giants (92-70, NL)
ALCS (4-1): Oakland Athletics vs. Toronto Blue Jays NLCS (4-1): San Francisco Giants vs. Chicago Cubs
1988 World Series (4-1): Los Angeles Dodgers (94-67, NL) vs. Oakland Athletics (104-58, AL)
ALCS (4-0): Oakland Athletics vs. Boston Red Sox NLCS (4-3): Los Angeles Dodgers vs. New York Mets
1987 World Series (4-3): Minnesota Twins (85-77, AL) vs. St. Louis Cardinals (95-67, NL)
ALCS (4-1): Minnesota Twins vs. Detroit Tigers NLCS (4-3): St. Louis Cardinals vs. San Francisco Giants
1986 World Series (4-3): New York Mets (108-54, NL) vs. Boston Red Sox (95-66, AL)
ALCS (4-3): Boston Red Sox vs. California Angels NLCS (4-2): New York Mets vs. Houston Astros
1985 World Series (4-3): Kansas City Royals (91-71, AL) vs. St. Louis Cardinals (101-61, NL)
ALCS (4-3): Kansas City Royals vs. Toronto Blue Jays NLCS (4-2): St. Louis Cardinals vs. Los Angeles Dodgers
1984 World Series (4-1): Detroit Tigers (104-58, AL) vs. San Diego Padres (92-70, NL)
ALCS (3-0): Detroit Tigers vs. Kansas City Royals NLCS (3-2): San Diego Padres vs. Chicago Cubs
1983 World Series (4-1): Baltimore Orioles (98-64, AL) vs. Philadelphia Phillies (90-72, NL)
ALCS (3-1): Baltimore Orioles vs. Chicago White Sox NLCS (3-1): Philadelphia Phillies vs. Los Angeles Dodgers
1982 World Series (4-3): St. Louis Cardinals (92-70, NL) vs. Milwaukee Brewers (95-67, AL)
ALCS (3-2): Milwaukee Brewers vs. California Angels NLCS (3-0): St. Louis Cardinals vs. Atlanta Braves
1981 World Series (4-2): Los Angeles Dodgers (63-47, NL) vs. New York Yankees (59-48, AL)
ALCS (3-0): New York Yankees vs. Oakland Athletics NLCS (3-2): Los Angeles Dodgers vs. Montreal Expos
ALDS (3-2): NYY vs. MIL ALDS (3-0): OAK vs. KCR NLDS (3-2): MON vs. PHI NLDS (3-2): LAD vs. HOU
1980 World Series (4-2): Philadelphia Phillies (91-71, NL) vs. Kansas City Royals (97-65, AL)
ALCS (3-0): Kansas City Royals vs. New York Yankees NLCS (3-2): Philadelphia Phillies vs. Houston Astros
1979 World Series (4-3): Pittsburgh Pirates (98-64, NL) vs. Baltimore Orioles (102-57, AL)
ALCS (3-1): Baltimore Orioles vs. California Angels NLCS (3-0): Pittsburgh Pirates vs. Cincinnati Reds
1978 World Series (4-2): New York Yankees (100-63, AL) vs. Los Angeles Dodgers (95-67, NL)
ALCS (3-1): New York Yankees vs. Kansas City Royals NLCS (3-1): Los Angeles Dodgers vs. Philadelphia Phillies
1976 World Series (4-0): Cincinnati Reds (102-60, NL) vs. New York Yankees (97-62, AL)
ALCS (3-2): New York Yankees vs. Kansas City Royals NLCS (3-0): Cincinnati Reds vs. Philadelphia Phillies
1975 World Series (4-3): Cincinnati Reds (108-54, NL) vs. Boston Red Sox (95-65, AL)
ALCS (3-0): Boston Red Sox vs. Oakland Athletics NLCS (3-0): Cincinnati Reds vs. Pittsburgh Pirates
1974 World Series (4-1): Oakland Athletics (90-72, AL) vs. Los Angeles Dodgers (102-60, NL)
ALCS (3-1): Oakland Athletics vs. Baltimore Orioles NLCS (3-1): Los Angeles Dodgers vs. Pittsburgh Pirates
1973 World Series (4-3): Oakland Athletics (94-68, AL) vs. New York Mets (82-79, NL)
ALCS (3-2): Oakland Athletics vs. Baltimore Orioles NLCS (3-2): New York Mets vs. Cincinnati Reds
1972 World Series (4-3): Oakland Athletics (93-62, AL) vs. Cincinnati Reds (95-59, NL)
ALCS (3-2): Oakland Athletics vs. Detroit Tigers NLCS (3-2): Cincinnati Reds vs. Pittsburgh Pirates
ALCS (3-0): Baltimore Orioles vs. Oakland Athletics NLCS (3-1): Pittsburgh Pirates vs. San Francisco Giants
1970 World Series (4-1): Baltimore Orioles (108-54, AL) vs. Cincinnati Reds (102-60, NL)
ALCS (3-0): Baltimore Orioles vs. Minnesota Twins NLCS (3-0): Cincinnati Reds vs. Pittsburgh Pirates
1969 World Series (4-1): New York Mets (100-62, NL) vs. Baltimore Orioles (109-53, AL)
ALCS (3-0): Baltimore Orioles vs. Minnesota Twins NLCS (3-0): New York Mets vs. Atlanta Braves
1968 World Series (4-3): Detroit Tigers (103-59, AL) vs. St. Louis Cardinals (97-65, NL)
1967 World Series (4-3): St. Louis Cardinals (101-60, NL) vs. Boston Red Sox (92-70, AL)
1966 World Series (4-0): Baltimore Orioles (97-63, AL) vs. Los Angeles Dodgers (95-67, NL)
1965 World Series (4-3): Los Angeles Dodgers (97-65, NL) vs. Minnesota Twins (102-60, AL)
1964 World Series (4-3): St. Louis Cardinals (93-69, NL) vs. New York Yankees (99-63, AL)
1963 World Series (4-0): Los Angeles Dodgers (99-63, NL) vs. New York Yankees (104-57, AL)
1962 World Series (4-3): New York Yankees (96-66, AL) vs. San Francisco Giants (103-62, NL)
1961 World Series (4-1): New York Yankees (109-53, AL) vs. Cincinnati Reds (93-61, NL)
1960 World Series (4-3): Pittsburgh Pirates (95-59, NL) vs. New York Yankees (97-57, AL)
1959 World Series (4-2): Los Angeles Dodgers (88-68, NL) vs. Chicago White Sox (94-60, AL)
1958 World Series (4-3): New York Yankees (92-62, AL) vs. Milwaukee Braves (92-62, NL)
1957 World Series (4-3): Milwaukee Braves (95-59, NL) vs. New York Yankees (98-56, AL)
1956 World Series (4-3): New York Yankees (97-57, AL) vs. Brooklyn Dodgers (93-61, NL)
1955 World Series (4-3): Brooklyn Dodgers (98-55, NL) vs. New York Yankees (96-58, AL)
1954 World Series (4-0): New York Giants (97-57, NL) vs. Cleveland Indians (111-43, AL)
1953 World Series (4-2): New York Yankees (99-52, AL) vs. Brooklyn Dodgers (105-49, NL)
1951 World Series (4-2): New York Yankees (98-56, AL) vs. New York Giants (98-59, NL)
1950 World Series (4-0): New York Yankees (98-56, AL) vs. Philadelphia Phillies (91-63, NL)
1948 World Series (4-2): Cleveland Indians (97-58, AL) vs. Boston Braves (91-62, NL)
1946 World Series (4-3): St. Louis Cardinals (98-58, NL) vs. Boston Red Sox (104-50, AL)
1945 World Series (4-3): Detroit Tigers (88-65, AL) vs. Chicago Cubs (98-56, NL)
1944 World Series (4-2): St. Louis Cardinals (105-49, NL) vs. St. Louis Browns (89-65, AL)
1943 World Series (4-1): New York Yankees (98-56, AL) vs. St. Louis Cardinals (105-49, NL)
1942 World Series (4-1): St. Louis Cardinals (106-48, NL) vs. New York Yankees (103-51, AL)
1941 World Series (4-1): New York Yankees (101-53, AL) vs. Brooklyn Dodgers (100-54, NL)
1940 World Series (4-3): Cincinnati Reds (100-53, NL) vs. Detroit Tigers (90-64, AL)
1938 World Series (4-0): New York Yankees (99-53, AL) vs. Chicago Cubs (89-63, NL)
1937 World Series (4-1): New York Yankees (102-52, AL) vs. New York Giants (95-57, NL)
1935 World Series (4-2): Detroit Tigers (93-58, AL) vs. Chicago Cubs (100-54, NL)
1934 World Series (4-3): St. Louis Cardinals (95-58, NL) vs. Detroit Tigers (101-53, AL)
1933 World Series (4-1): New York Giants (91-61, NL) vs. Washington Senators (99-53, AL)
1932 World Series (4-0): New York Yankees (107-47, AL) vs. Chicago Cubs (90-64, NL)
1931 World Series (4-3): St. Louis Cardinals (101-53, NL) vs. Philadelphia Athletics (107-45, AL)
1930 World Series (4-2): Philadelphia Athletics (102-52, AL) vs. St. Louis Cardinals (92-62, NL)
1929 World Series (4-1): Philadelphia Athletics (104-46, AL) vs. Chicago Cubs (98-54, NL)
1928 World Series (4-0): New York Yankees (101-53, AL) vs. St. Louis Cardinals (95-59, NL)
1927 World Series (4-0): New York Yankees (110-44, AL) vs. Pittsburgh Pirates (94-60, NL)
1925 World Series (4-3): Pittsburgh Pirates (95-58, NL) vs. Washington Senators (96-55, AL)
1924 World Series (4-3): Washington Senators (92-62, AL) vs. New York Giants (93-60, NL)
1922 World Series (4-0-1): New York Giants (93-61, NL) vs. New York Yankees (94-60, AL)
1921 World Series (5-3): New York Giants (94-59, NL) vs. New York Yankees (98-55, AL)
1920 World Series (5-2): Cleveland Indians (98-56, AL) vs. Brooklyn Robins (93-61, NL)
1919 World Series (5-3): Cincinnati Reds (96-44, NL) vs. Chicago White Sox (88-52, AL)
1918 World Series (4-2): Boston Red Sox (75-51, AL) vs. Chicago Cubs (84-45, NL)
1917 World Series (4-2): Chicago White Sox (100-54, AL) vs. New York Giants (98-56, NL)
1916 World Series (4-1): Boston Red Sox (91-63, AL) vs. Brooklyn Robins (94-60, NL)
1915 World Series (4-1): Boston Red Sox (101-50, AL) vs. Philadelphia Phillies (90-62, NL)
1914 World Series (4-0): Boston Braves (94-59, NL) vs. Philadelphia Athletics (99-53, AL)
1913 World Series (4-1): Philadelphia Athletics (96-57, AL) vs. New York Giants (101-51, NL)
1912 World Series (4-3-1): Boston Red Sox (105-47, AL) vs. New York Giants (103-48, NL)
1911 World Series (4-2): Philadelphia Athletics (101-50, AL) vs. New York Giants (99-54, NL)
1910 World Series (4-1): Philadelphia Athletics (102-48, AL) vs. Chicago Cubs (104-50, NL)
1909 World Series (4-3): Pittsburgh Pirates (110-42, NL) vs. Detroit Tigers (98-54, AL)
1908 World Series (4-1): Chicago Cubs (99-55, NL) vs. Detroit Tigers (90-63, AL)
1907 World Series (4-0-1): Chicago Cubs (107-45, NL) vs. Detroit Tigers (92-58, AL)
1906 World Series (4-2): Chicago White Sox (93-58, AL) vs. Chicago Cubs (116-36, NL)
1905 World Series (4-1): New York Giants (105-48, NL) vs. Philadelphia Athletics (92-56, AL)
1903 World Series (5-3): Boston Americans (91-47, AL) vs. Pittsburgh Pirates (91-49, NL)
Post-season games prior to 1903 were considered exhibitions.
1892 Championship Series (5-0-1): Boston Beaneaters (102-48, NL) vs. Cleveland Spiders (93-56, NL)
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text:
Year : 2012 | Volume : 1 | Issue : 2 | Page : 99-105
Quantitative and qualitative analysis of collagen in oral submucous fibrosis
Gannepalli Ashalata, Pacha Venkat Baghirath, Ayinampudi Bhargavi Krishna, Putcha Uday Kumar, Arun Tom
Department of Oral & Maxillofacial Pathology, Panineeya Mahavidyalaya Institute of Dental Sciences & Research Centre, Dilshukhnagar, Hyderabad, Andhra Pradesh, India
Date of Web Publication 11-Jul-2012
Gannepalli Ashalata
Professor, Department of Oral & Maxillofacial Pathology, Panineeya Mahavidyalaya Institute of Dental Sciences & Research Centre, Road No.5, Kamala Nagar, Dilshukhnagar, Hyderabad, Andhra Pradesh - 500060
Background: Oral submucous fibrosis (OSMF) is considered as a potentially malignant disease, which is associated with betel quid and pan masala chewing. It is thought to be due to the defective collagen synthesis and degradation. The amount of collagen in the diseased varies with the functional stages and histopathological grades of the disease.
Aims: The aim of the study was to assess the severity of the disease in oral submucous fibrosis, by correlating the functional staging with the histopathological grading and analyze the collagen distribution in different grades of OSMF using picrosirius red stain under polarizing microscope and also to assess the quantitative changes in collagen with respect to various histopathological grades of OSMF using spectrophotometry.
Materials and Methods: The study conducted on 40 subjects, which included 30 subjects with different functional and histopathological grades of oral submucous fibrosis (OSMF), and 10 were in control group. Functional staging and histopathological grading was done based on the definite criteria. A Histopathological and quantitative analysis of collagen was conducted using picrosirius red stain, polarizing microscope and spectrophotometer, respectively. The results were analyzed using chi-square test, and the significance was tabulated.
Results: The functional staging and the histopathological grading did not show statistical correlation, but as the histopathological grade of the disease increased; there was a shift in the polarizing color from yellow-green to orange-red. In the colorimetric estimation, the optical densities of the sample decreased as with increased grades of OSMF.
Conclusion: In the present study, we observed that the histopathological grading of OSMF is not correlating with the functional staging of OSMF. Therefore, it mandates the proper correlation between the functional staging and the histopathological grading before the commencement of the treatment to render better outcome of the treatment.
Keywords: Collagen, oral submucous fibrosis, polarizing microscope, picrosirius red, spectrophotometry
Ashalata G, Baghirath PV, Krishna AB, Kumar PU, Tom A. Quantitative and qualitative analysis of collagen in oral submucous fibrosis. J NTR Univ Health Sci 2012;1:99-105
Ashalata G, Baghirath PV, Krishna AB, Kumar PU, Tom A. Quantitative and qualitative analysis of collagen in oral submucous fibrosis. J NTR Univ Health Sci [serial online] 2012 [cited 2020 Jan 19];1:99-105. Available from: http://www.jdrntruhs.org/text.asp?2012/1/2/99/98350
In 1952, Schwartz described 5 Indian women at Kenya with a condition of the oral mucosa including the palate and pillars of the fauces, which he called "atrophia idiopathica." Later, it was termed oral submucous fibrosis (OSMF). Other names for this condition are "diffuse oral submucous fibrosis, idiopathic scleroderma of the mouth, idiopathic palatal fibrosis, sclerosing stomatisis, and juxta-epithelial fibrosis." [1]
The number of cases of OSMF has raised rapidly in India from an estimated 250,000 cases in 1980 to 2 million cases in 1993 with an overall prevalence rate of 0.2% to 0.5% and prevalence by gender varying from 0.2 to 2.3% in males and 1.2 to 4.57% in females. [2],[3] The age of occurrence for OSMF is ranging between 20 and 40 years of age. [4] It has been suggested that areca nut chewing, ingestion of chilies, genetic susceptibility, nutritional deficiencies, altered salivary constituents, autoimmunity and collagen disorders may be involved in the pathogenesis of this condition. [1],[5] The chewing of betel quid (BQ) and pan masala has been recognized as the one of the most important risk factors for OSMF as per the recent epidemiological data. [5]
The possible precancerous nature of OSMF was first mentioned by Paymaster who described among patients in Bombay, the development of slow growing squamous cell carcinoma in a third of the patients with OSMF. [4] It is now considered as a potentially malignant disorder with an overall transformation rate of 7.6% over a period of 17 years, among the Indian population. [6]
Various histopathological, immunological, and electron microscopic studies have shown that the pathogenesis of OSMF is associated with the increase in the deposition of extracellular matrix (ECM) by increasing the matrix proteins like collagen and decreasing its degradation by various inhibitory mechanisms. [5] The clinical and histopathological grades of OSMF varies with the amount of collagen present in the ECM, major studies have been focused on the qualitative assessment of the collagen fibers in OSMF. Hence, in the present study, we made an attempt to correlate between the functional staging and histopathological grading and different histopathological grades with respect to the qualitative and quantitative analysis of collagen.
The study group comprised of 30 patients with clinical signs and symptoms of OSMF and 10 subjects in the control group who were devoid of any symptoms and any other systemic disorders. An incisional biopsy was performed after obtaining the written consent from all subjects. OSMF cases were clinically categorized into subjects in the study group were grouped functionally based on the criteria by Kiran et al as given below [Figure 1]: [7]
Figure 1: Showing reduced mouth opening (Stage 3 OSMF)
Stage 1: Mouth opening ≥45 mm
Stage 2: Restricted mouth opening 20-44 mm
Stage 3: Mouth opening ≤20 mm
The hematoxylin and eosin (H and E) stained sections were viewed under the light microscope for the histopathologic grading based on the criteria, which were modified from the original criteria given by Pindborg and Sirsat as given below: [8]
Grade 1: Early hyalinization of juxtaepithelial area, plump young fibroblasts, dilated or congested blood vessels, and presence of inflammatory cells mostly mononuclear lymphocytes, eosinophils, and occasional plasma cells.
Grade 2: Moderately hyalinized collagen, less marked fibroblastic response, presence of mostly fibrocytes, constricted blood vessels, and inflammatory exudate consist of mostly lymphocytes and plasma cells with occasional eosinophils.
Grade 3: Complete hyalinization of collagen with depletion of fibroblasts in those areas, blood vessels are completely obliterated or narrowed, and inflammatory cells are lymphocytes and plasma cells [Figure 2].
Figure 2: Image showing complete hyalinization of the extracellular matrix and loss of rete ridges
Procedure for polarizing microscopy
The paraffin-embedded tissues were cut into 5 mm thick sections and were stained using Picrosirius red stain. The stained sections were examined under a polarizing microscope to observe the polarizing colors of the collagen fibers in the connective tissue. On considering the variable thickness of normal mucosal collagen fibers as 1-12 mm, collagen fibers with thickness less than or equal to 5 mm were considered as thin fibers and those with more than 5 mm, was considered as thick fibers. The connective tissue was divided into upper half, immediately below the basal lamina and lower half, immediately above the sub mucosa, and a total of 5 randomly selected high power (100 ×) fields were examined in each half, and the mean was considered as the number of fibers pertaining to that area. Only well discernible and distinct fibers were selected in each field. The same procedure was adopted for the control group also.
The thickness and color of the collagen fibers were measured and analyzed using the image analysis software Sigma scan pro 5.
Colorimetric quantification of collagen
The paraffin-embedded sections of 10 μm thicknesses were placed on the glass slide, deparaffinized and stained with 0.1% picrosirius red saturated with picric acid for 30 min in the dark, at ambient temperature. After staining, the sections were rinsed several times with distilled water, and with the help of shaving blade, sections were agglomerated to an assay tube which contained 1 ml of solution of 0.1% of NaOH in absolute methanol (1:1, v:v) to wash out the bound dye from the sections. The absorbency of the washed tissue was read in a spectrophotometer at 540 nm. This absorbency refers to the collagen content in the specimens. As the collagen content of the sample increases, the absorbency decreases.
Statistical analysis was done using Medi calc software, Chi square test was done to compare the significance between various groups at the level of significance 0.5.
Total study group was comprised of 30 subjects of OSMF with different functional stages and histopathological grades of OSMF and 10 in the control group. The age group in the study group was ranging from 18 to 37 years with the mean age of 27.13 years and for the control group, 22 to 28 years with the mean age of 26.4 years.
Functional staging of the study group was done based on the mouth opening. Stage 1 comprised of 2 cases, stage 2 comprised of 18 cases, and stage 3 comprised of 10 cases [Table 1]. The experimental group was divided into 3 groups based on the histopathological grading based on the defined criteria, grade 1 comprised of 10 cases, grade 2 comprised of 10 cases, and grade 3 comprised of 10 cases [Table 2].
Table 1: Showing total number of cases with respect to the functional stages
Table 2: Showing total number of cases with respect to the histopathological grading
Comparison between the functional staging and the histopathological grading did not show any statistical significance (P = 0.0663) [Table 3].
Table 3: Showing comparison between functional staging and the histopathological grading
Polarizing microscopic evaluation
The study of the tissue sections in the upper half of the connective tissue revealed that the number of thin fibers with green-grey color decreased in number and the orange-red color increased as the grade of the disease progressed and the number of thick fibers with green-grey color decreased and the orange-red color increased as the grade of the disease advances, and the result obtained was significant (P < 0.001) [Figure 3], [Figure 4], [Figure 5] and [Figure 6], [Table 4] and [Table 5].
Figure 3: Polarizing photomicrograph showing the upper half of the connective tissue from the normal buccal mucosa
Figure 4: Polarizing photomicrograph showing the upper half of the connective tissue in grade 1 OSMF
Table 4: Showing average number of thin fibers in the upper half of the connective tissue
Table 5: Showing the average number of the thick fibers in the upper half of the connective tissue
In the lower half, the thin fibers showed the reduction of green-grey color and a considerable increase in the number of orange-red fibers as with the progress of disease severity. Also, for the thick fibers, the number of green-grey fibers reduced and the orange-red fibers increased as the grade of disease progressed, and the obtained result showed high significance (P < 0.001) [Figure 7], [Figure 8], [Figure 9] and [Figure 10], [Table 6] and [Table 7].
Figure 7: Polarizing photomicrograph showing the lower half of the connective tissue in normal buccal mucosa
Figure 8: Polarizing photomicrograph showing the lower half of the connective tissue in grade 1 OSMF
Figure 10: Polarizing photomicrograph showing the lower half of the connective tissue in grade 3 OSMF
Table 6: Showing the average number of the thin fibers in the lower half of the connective tissue
Table 7: Showing the average number of the thick fibers in the lower half of the connective tissue
Colorimetric analysis
The colorimetric evaluation of collagen revealed a progressive reduction in the optical densities as the disease grade increased. The result obtained was statistically significant (P < 0.001) [Table 8], [Graph 1].
Table 8: Showing the comparison between the histopathological grading and the derived optical densities from spectrophotometry
The cause of increased collagen deposition in the connective tissue in OSMF is directly attributed to the effect of areca nut (betel nut) component of the betel quid, which cause an abnormal increase in the deposition of collagen. [9],[10] The alkaloids and the flavonoids present in the areca nut have shown to exert a stimulatory effect on the buccal mucosal fibroblasts and thus resulting in the accumulation of collagen. This collagen accumulation is directly attributed to the increased collagen cross linking, which in-turn result in reduced collagen degradation along with the reduced collagenase activity. [5]
Recent studies on pathogenesis of OSMF revealed that the arecaidine, a product formed due to the hydrolysis of arecoline, along with copper results in fibroblast stimulation. Along with the increased fibroblast production, the tannins which is another constituent of the areca nut leads to the stabilization of the collagen structure. [2]
Many of the previous studies conducted OSMF to correlate between the clinical staging and the histopathological grading did not show any significant correlation. [7],[8],[11],[12] As the major criteria used in our clinical practice in establishing the treatment protocol for the OSMF patients is the functional staging, but in the present study, the correlation between the functional staging and histopathological grading was not significant, especially between stage 2 and grade 2. It could be due to the fact that the initial fibrosis beginning at the fauces, followed by buccal and labial areas. [13] The preferred biopsy site in our study was the buccal mucosa and due to the inaccessibility of the surgeon to the posterior most areas near the fauces, which could shift most of the stage 1 cases to stage 2, or it could be due to the fact that physiological range of mouth opening varies in different individuals which in turn affect the rate of decreased mouth opening due to the disease. Hence, we correlated histopathological grading with the advanced aids like polarizing microscopy and spectrophotometry, which estimates collagen qualitatively and quantitatively.
The upper and the lower half of the connective tissue revealed that the number of thick and thin orange red fibers increased as the grade of the disease progressed. The possible reason for this finding could be due to the increased collagen cross linking which in-turn result in reduced collagen degradation along with the reduced collagenase activity as the disease progressed. [5] In the advanced stages of the disease, the collagen fibers appeared to be highly hyalinized and the delineation between the fibers was difficult. This tight packing of the collagen fibers could be the other reason for appearance of orange-red color. [11]
When comparing with the upper half of the connective tissue, there was a statistically significant increase in the number of thick fibers in lower half in the study group. It could be due to the commencement of the initial fibrosis in the lower sub mucosa compared to the upper and also may be due to the presence of more healthy and thick collagen fibers and bundles in the submucosa. [14],[15]
There was a progressive reduction in the optical densities in the colorimetric evaluation; the possible reason for this could be the increase in the amount of collagen as the grade of the disease progress and which results in the increased intake of the stain. The increased amount of the stain in the fluid, which is read in the spectrophotometer, results in increased absorbance of the photons which in turn results in the reduction of the optical densities. [16],[17]
In conclusion, the present study revealed that the current criteria used in the clinics for the treatment i.e., functional staging, is showing no correlation with the histopathological grading. We could establish a positive correlation with the histopathological grading to the quantity and quality of collagen present in different grades of OSMF. This fact, therefore, necessitate the need of proper histopathological grading of the disease before commencing the treatment, which could result in better outcome for the treatment and prevent further malignant transformation.
1. Rajendran R. Oral submucous fibrosis: Etiology, pathogenesis, and future research. Bull World Health Organ 1994;72:985-96.
2. Tilakaratne WM, Kinikowski MF, Saku T, Peters TJ, Warnakulasuriya S. Oral submucous fibrosis: Review on aetiology and pathogenesis. Oral Oncol 2006;42:561-8.
3. Reddy V, Wanjari PV, Banda NR, Reddy P. Oral submucous fibrosis: Correlation of clinical grading to various habit factors. International Journal of Dental Clinics 2011;3:21-24.
4. Pindborg JJ. Oral submucous fibrosis as a precancerous condition. J Dent Res. 196645 (Suppl 3):546-53.
5. Rajalalitha P, Vali S. Molecular pathogenesis of oral submucous fibrosis - a collagen metabolic disorder. J Oral Pathol Med 2005;34:321- 8.
6. Murti PR, Bhonsle RB, Pindborg JJ, Daftary DK, Gupta PC, Mehta FS. Malignant transformation rate in oral submucous fibrosis over a 17- year period. Community Dent Oral Epidemiol 1985;13:340-1.
7. Kiran KK, Saraswathi TR, Ranganathan K, Uma Devi M, Joshua E. Oral submucous fibrosis: A clinic-histopathological study in Chennai. Indian J Dent Res 2007;18:106-11.
8. Shruthi P, Ajay KC, Mamta S, Mangal S, Ravi M. Correlation of histopathological diagnosis with habits and clinical findings in oral submucous fibrosis. Head Neck Oncol 2009;1-10.
9. Canniff JP, Harvey W. The aetiology of oral submucous fibrosis: The stimulation of collagen synthesis by extracts of areca nut. Int J Oral Surg 1981;10:163-7.
10. Harvey W, Scutt A, Meghji S, Canniff JP. Stimulation of human buccal mucosa fibroblasts in vitro by betel-nut alkaloids. Arch Oral Biol 1986;31:45-9.
11. Ceena DE, Bastian TS, Ashok L, Rajeswari GA. Comparative study of clinicofunctional staging of oral submucous fibrosis with qualitative analysis of collagen fibres under polarizing microscopy. Indian J Dent Res 2009;20:271-6.
12. Saurabh G, Junaid A, Mohit PS, Prashant N. Oral submucous fibrosis: A clinico-histopathological comparative study in population of Southern Rajasthan. J Carcinogene Mutagene 2010;1.
13. Haider SM, Merchant AT, Fikree FF, Rahbar MH. Clinical and functional staging of oral submucous fibrosis. Br J Oral Maxillofac Surg 2000;38:12-5.
14. Anna PJ, Rajendran R. Submucosa precedes lamina propria in initiating fibrosis in oral submucous fibrosis -evidence based on collagen histochemistry. Oral Maxillofac Pathol 2010;1.
15. Van Wyk CW, Seedat HA, Philips VM. Collagen in submucous fibrosis: An electron-microscopic study. J Oral Pathol Med 1990;19:182-9.
16. Rodrigues Jr AJ, Rodrigues CJ, da Cunha AC, Jin Y. Quantitative analysis of collagen and elastic fibres in the transversalis fascia in direct and indirect inguinal hernia. Rev Hosp Clin Fac Med Sao Paulo 2002;57:265-70.
17. Finkelstein I, Trope GE, Basu PK, Hasany SM, Hunter WS. Quantitative analysis of collagen content and aminoacids in trabecular meshwork. Br J Ophthalmol 1990;74:280-2.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8]
1 Polarized microscope assisted study of collagen fibres in Oral Submucous Fibrosis and their clinicopathologic correlation: An in-vitro study
Ameena Singh,Sukumar Singh,Susmita Saxena,Sanjeev Kumar,Akanksha Banga,Nitin Purohit
Journal of Oral Biology and Craniofacial Research. 2017;
Ashalata G
Baghirath PV
Krishna AB
Kumar PU
Tom A
oral submucous fibrosis
polarizing microscope
picrosirius red


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He specialises in (international) commercial law, distribution law (including franchising law) and market practices (including advertising, labelling and packaging). He both advises clients in these fields and represents them in related court and arbitration proceedings.
Filip has been a member of the Brussels Bar since 2010.
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text:
Jason Collins Signs With Nets And Becomes First Openly Gay Active Player In NBA History
By Chris Greenberg
Jason Collins is making a historic return to the NBA.
The 35-year-old NBA veteran is set to become the first openly gay professional athlete to compete in any of the four major North American team sports leagues -- NFL, MLB, NHL and NBA -- after signing a 10-day contract with the Brooklyn Nets. The landmark signing was announced by Nets general manager Billy King on Sunday afternoon and comes 10 months after Collins came out. With the Nets in Los Angeles to face the Lakers, King indicated that Collins will be available to play on Sunday evening.
"Right now, I'm focused on trying to learn the plays, trying to learn the coverages, the game plan, assignments," Collins told reporters during a press conference at Staples Center before the game. "I don't have time to really think about history right now. I just have to focus on my job tonight."
RT to welcome @jasoncollins34 to Brooklyn! #Nets pic.twitter.com/D05R9td9cx
— Brooklyn Nets (@BrooklynNets) February 23, 2014
The 7-foot center brings size to a roster lacking frontcourt depth since trading away forward Reggie Evans at the NBA trade deadline earlier this month. Collins has career averages of 3.6 points and 3.8 rebounds per game. He posted career-best averages of 6.4 points and 6.1 rebounds during the 2004-2005 campaign with the Nets. Known as a rugged interior defender, he also led the NBA in personal fouls (322) that season.
"The decision to sign Jason was a basketball decision," King said in a statement announcing Collins' signing. "We needed to increase our depth inside, and with his experience and size, we felt he was the right choice for a 10-day contract."
Collins has not played in the NBA since publicly announcing that he is gay in April 2013. A free agent when he came out in a moving first-person article in Sports Illustrated, Collins was not signed by any NBA team at the start of the 2013-2014 season. The 18th overall selection in the 2001 NBA Draft out of Stanford, Collins spent the first six full seasons of his career with the Nets before being traded to the Memphis Grizzlies during the 2007-2008 season. A role player at age 34, Collins appeared in just 38 games during the 2012-2013 season for the Washington Wizards and Boston Celtics.
"Jason told us that his goal was to earn another contract with an NBA team. Today, I want to commend him on achieving his goal," NBA Commissioner Adam Silver said in a statement. "I know everyone in the NBA family is excited for him and proud that our league fosters an inclusive and respectful environment."
The 12-season veteran joins a Nets roster filled with familiar faces. Not only was Collins a longtime teammate of Nets head coach Jason Kidd but he also previously played with Kevin Garnett, Paul Pierce and Joe Johnson. Collins' once and future teammates were expressing their support for signing him before the deal was announced.
"We would accept it greatly and it shouldn't be a problem, man," Johnson told Rod Boone of Newsday when asked about the possibility of signing Collins. "We've got a veteran group and I think everybody is pretty comfortable in their own skin. It's about what he can do to help us out there on that court. That's what it's about."
Collins signed with the Nets one day after All-American defensive lineman Michael Sam faced the media at the annual NFL Combine. Sam, who publicly revealed that he is gay in interviews with ESPN and The New York Times less than two weeks earlier, is poised to become the first openly gay player in NFL history. Not long after Collins came out in April 2013, former U.S. national team soccer player Robbie Rogers became the first openly gay athlete to play in the MLS when he made his debut with the L.A. Galaxy.
"Today, Jason Collins tore open the last remaining closet in America, and became the first openly gay player to be signed by a team in one of the big four sports," Brian Ellner, a member of the Athlete Ally board of directors, said in a statement released to ESPN. "We are especially excited that Jason will be playing in Brooklyn, just like Jackie Robinson, and in a marriage equality state. This is a piece of history, an important point on the continuum toward justice and a moment to celebrate."
When Collins resumes his NBA career, he will again wear No. 98, reported Ramona Shelburne of ESPN Los Angeles. In his heartfelt coming out editorial published in Sports Illustrated, Collins revealed the significance of the uniform number.
"My one small gesture of solidarity was to wear jersey number 98 with the Celtics and then the Wizards," Collins wrote. "The number has great significance to the gay community. One of the most notorious antigay hate crimes occurred in 1998. Matthew Shepard, a University of Wyoming student, was kidnapped, tortured and lashed to a prairie fence. He died five days after he was finally found. That same year the Trevor Project was founded. This amazing organization provides crisis intervention and suicide prevention to kids struggling with their sexual identity. Trust me, I know that struggle. I've struggled with some insane logic. When I put on my jersey I was making a statement to myself, my family and my friends."
Chris Greenberg
Sports Editor, The Huffington Post
Jason Collins Brooklyn Nets Gay Athletes Sports NBA


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Makanlah.com - New website for Food Lovers- Feedback and Join!
Thread: Makanlah.com - New website for Food Lovers- Feedback and Join!
Cheers. Please feedback as we are just new! Bugs might be here and there, we will try our best to solve it! Thanks !!
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text:
House of Wax (1953) / Mystery of the Wax Museum (1933)
41K ratings
item number: 35A55
Also released as:
House of Wax 3D (Blu-ray) for $20.20
More products that might interest you:
Classic Horror Collection: 20 Full Color Vintage Movie Postcards (Movie Collectible) $4.78
House of Wax Premiere Newsreel
House of Wax Languages: English, French and Spanish House of Wax Subtitles in English, French, Spanish, Portuguese, Japanese, Chinese, Bahasa, Thai & Korean Mystery of the Wax Museum Subtitles in English, French and Spanish
Closed captioning available
Released: August 5, 2003
Packaging: Snap Case
Mono - English
Mono - Spanish
Starring Vincent Price, Frank Lovejoy & Phyllis Kirk
Performer: Carolyn Jones, Charles Bronson, Paul Picerni, Roy Roberts, Angela Clarke, Paul Cavanagh & Dabbs Greer
Directed by André De Toth
Edited by Rudi Fehr
Screenplay by Crane Wilbur
Composition by David Buttolph
Art Direction by Stanley Fleischer
Story by Charles S. Belden
Produced by Bryan Foy
Director of Photography: Bert Glennon & J. Peverell Marley
Total Count: 41
Unlike many of the hastily assembled 3-D projects that followed it, HOUSE OF WAX was carefully designed to take maximum advantage of the medium's unusual properties. The film employs a full range of imaginative shock effects...
An intermittently gripping shocker. Full Review
The effects are done with playfulness, zest, and some imagination (they range from a barker batting paddleballs in your face to a murderer leaping from the row in front of you), making this the most entertaining of the gimmick 3-Ds. Full Review
Casting is competent, Vincent Price is capital as the No. 1 menace. Full Review
[O]ne of the most popular 3-D movies...
...Great fun...
Rating: 7/10 -- In any number of dimensions, it's a delightfully garish exercise in low-grade creeps. Full Review
Antagony & Ecstasy
In the wicked performance that crowned him the movie's master of the macabre. Vincent Price plays a renowned wax sculptor plunged into madness when an arsonist destroys his life's work. Unable to use his flame-scarred hands, he devises a new - and murderous - way of restocking his House of Wax.
The sweet dread and sheer fun of this creepy classic, co-starring Phyllis Kirk, Carolyn Jones and Charles Bronson and directed by Andre de Toth, had its roots in a Warner Bros. chiller from 20 years before: Mystery of the Wax Museum, starring Lionel Atwill as the wax-wielding madman and Fay Wray as a potential victim. Directed by Michael Curtiz and shot in a chillingly effective early two-color Technicolor process, it and its spooky remake offer you a delicious double-dip in a paraffin bath of terror.
André de Toth's remake of MYSTERY OF THE WAX MUSEUM is one of the first and best 3-D (stereoscopic) feature films, an alternative technology (like Cinemascope, Cinerama) used by 1950s directors attempting to compete with the new threat of television. Professor Jarrod (Vincent Price) is a devoted wax figure sculptor for his museum in 1910s NYC. When his financial partner, Sidney Wallace (Paul Cavanagh), demands more sensational exhibits to increase profits, Jarrod refuses. The vengeful Wallace torches the museum, leaving Jarrod for dead. Miraculously, Jarrod survives (though his hands and legs are rendered useless) and builds a new House of Wax with help from threatening deaf-mute sculptor, Igor (Charles Bronson). The museum's popular "Chamber of Horrors" showcases recent crimes like the murder of Wallace, a victim of a cloaked, disfigured killer along with his fiancée, Cathy (Carolyn Jones). When Cathy's friend, Sue (Phyllis Kirk), visits the museum she makes a discovery that leads to the horrifying truth behind the House of Wax. With gasp inducing (and tongue-in-cheek) 3-D scenes like the museum fire, paddleball man, and can-can girls, de Toth creates an atmospheric film which stands up as a horror classic in 2-D as well.
Psychos | Murder | Art / Artists | Theatrical Release
Production Notes:
When theatrically re-issued, "House of Wax" received an MPAA GP rating.
Filmed in Technicolor and Stereophonic sound.
Rated BBFC PG by the British Board of Film Classification.
Andre de Toth had one eye while directing the film and was unable to enjoy the groundbreaking 3-D effects.
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This 300 AAC Blackout cartridge by Fiocchi is capped off with a 220 grain bullet, the heft of which assures that its muzzle velocity will always hover below what it would take to shatter the sound barrier. The softer report of subsonic ammunition like this is still markedly audible, but it does a fine job of making your target shooting session far less conspicuous. It's also great for introducing easily startled neophytes to the world of marksmanship, and it barely registers a squeak when fired from a silenced firearm.
Its low muzzle velocity doesn't greatly impact this round's accuracy, because it's outfitted with a Sierra MatchKing projectile. The bullet sports a boat tail design, so its ballistic coefficient is high enough to ensure a flat trajectory, superior velocity retention downrange, and greater immunity to wind drift. This bullet's jacket is highly concentric to improve its rotational stability, and its hollow point meplat is narrow to further improve its aerodynamic profile.


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KSGC may refer to:

 KSGC-LP, a low-power radio station (100.5 FM) licensed to serve Garden City, Kansas, United States
 KSGC (defunct), a defunct radio station (92.1 FM) formerly licensed to serve Tusayan, Arizona, United States

redpajama_set_name: RedPajamaWikipedia