Friday, July 27, 2012

An Analysis of ADA

C-SPAN (Washington Journal) is currently showing a program about ADA.  Tom Harkin, who sponsored it, has noted that it hasn't done a damn thing to increase employment among the disabled -- still, 60% of the disabled are unemployed.
Just because I have the legal right to a job does not mean that I can get one.  Employers are still resistant to hiring the disabled.  As happened to me once, they'll add something to the job description (in that instance, "must speak Chinese") so that they're turning you down for reasons other than your disability.  Once they added that extra (unnecessary) item, I was no longer qualified for the job.
There are plenty of jobs that COULD be done from home, but employers are afraid you'll goof off instead of working, so they won't hire you to work from home. 
In my case, if I have to report to an office rather than working from bed, I need "work when able", which the court has held is NOT an ADA-mandated accommodation; someone who needs a flexible schedule can't insist on it.
Someone's just written in with the observation that it's not so easy to get on Disability.  Let's see whether that sinks in with any of these closed-minded people calling and commenting about the number of fakers.  It took me 11 years, almost to the day, from the day I lost my job until the day I was approved for SSDI.  It's simply not as easy as walking in and saying "I'm disabled, gimme money."
"It's the one minority group that everyone can join." 
     -- Curtis Decker,
        Executive Director, 
        National Disability Rights Network
Video and/or transcripts should be available later at:

Whittemore Trial Postponed

Source: Reno Gazette Journal
Date:   July 2, 2012
Author:  Martha Bellisle

Harvey  Whittemore trial on illegal campaign finance charges  postponed

The  Aug. 7 federal trial for embattled lobbyist-developer Harvey
Whittemore,  charged with making illegal campaign contributions to U.S.
Senate Majority  Leader Harry Reid and lying to federal officials, has
been postponed. U.S.  District Judge Larry Hicks issued an order
Wednesday granting requests by  Whittemore's lawyers and prosecutors to
delay the trial until the end of the  year or early in 2013. In a
motion filed Tuesday, Whittemore's lawyers said  they needed more time
to prepare for the trial and prosecutors said they did  not object to a
delay. 'The government entered into a stipulation with  defense counsel
requesting that the court vacate the trial date and the date  for
pretrial motions and set a hearing to determine the trial date,' 
Natalie Collins, spokeswoman for the U.S. Attorney's Office, wrote in
an  email.

The defense asked for more time to prepare and asked for a  continuance
until June 2013, she said. 'The government believes that a June  2013
date is an unreasonable length of time given the nature of this case, 
and will not oppose a continuance of a trial date to a time between 
December 1, 2012 and February 28, 2013,' she said in the email.

Hicks  said he would hear arguments on setting a new trial at a later
date. No date  was specified by Wednesday. Dominic Gentile,
Whittemore's Las Vegas lawyer,  said he was pleased with Hicks'
decision, adding that he is preparing for  two other trials 'and it was
not going to be possible to be ready for this  one in time.' Gentile
said Whittemore has continued to work in Reno, 'but  he's not as happy
as he used to be. 'Other than that, life goes on,' he  said.

Pain -- the Fifth Vital Sign

Pain, The Fifth Vital Sign    Got this handout at the Awareness Day rally -- thanks to Jeanne Hess, RN      0 Absence of discomfort    1 Mild pain. Under your conscious radar. Does not interfere with  ability to concentrate or perform activities.    2 Discomforting pain. You are periodically aware of discomfort, which  subsides with rest, distraction (pleasant activity, music, conversation),  change of position, etc.    3 Tolerable, yet annoying pain. NOW is the time to treat with  medication in conjunction with comfort measures. Allows best opportunity for  effective pain control with the least medication.    4 Pain has your full attention now. "Why didn't I initiate comfort  measures and medication sooner?"    5 Moderate pain. Constant, sometimes nauseating pain. Lack of  appetite, difficulty concentrating. Begin to isolate self from noise, activity.    6 Grueling, numbing pain. Body tense. Nausea, intolerance for cold,  noise and activity increase, mood sinks and increased withdrawal. "Leave me  alone."    7 Miserable, agonizing, gnawing pain. "When is SOMETHING going to  help?"    8 Horrible, vicious pain. Jaws clenched, respirations rapid &  shallow. "WHY isn't anything helping?"    9 Consumed by torturing, crushing unbearable pain. "Get me help NOW!"    10 Physiologically intolerable pain. Loss of consciousness.            

10 Reasons to Use Caution With Pain Relievers - CNN

However, if you DON'T relieve pain, you may be creating a chronic pain syndrome like fibromyalgia. 
Treat AHEAD of the pain; don't wait till it gets to level 9 or 10 and then try to play catch-up, because you can't.

Wednesday, July 25, 2012

Job Hunting with a Disability

If you are actively job hunting and have a disability, Think Beyond the Label is putting together some fabulous hiring opportunities for you in the very near future! Employers from startups to Fortune-500s will be participating in search of dedicated workers who bring talent and diversity their workforce. To be part of these, be sure to register at the link below!

Too good to be true

I've had problems for 15 years with the city trash service.  Even if I put the can exactly where they want it, it's hit-and-miss whether it gets emptied (and sometimes "emptied" is a relative term; they only dump a small portion of it).
Since I have a bad back and shouldn't be carrying anything, and have neurological problems that make the stairs dangerous, I was very happy last month to find out that they have Disabled Trash Service, in which they will take your can to the curb for you.
Today was the first day that I was supposed to get it, and instead I got a visit from a lower-level supervisor informing me that they won't come up the stairs to get my trash.  I have to figure out myself how to get the trash down the stairs, which is the problem that I applied for help with in the first place.  Once I've taken it more than halfway from my front door to the curb, they'll be happy to move it the last few feet.
The neighbors would rather insult me than help me, so that's not an option.  I was advised that if I throw the bags down the stairs and they burst, it is not the city's responsibility to clean up the mess.
Apparently, my only option is to hire someone (a handyman @$25+/visit?) to carry the trash down the stairs for me.

The truth about sugar

high fructose corn syrup. It has proven to be a low-cost and efficient sweetener in many products but has also been targeted by activists and food elitists as a major cause of obesity.

The notion is absurd. Sugar from corn has not been shown to be different from other sugar in terms of sweetness, eliciting insulin release or the feeling of satiety after eating. All are metabolized in the same fashion and provide four calories per gram.

* * *

Dr. Bruno notes that CFS patients tend toward hypoglycemia (low blood sugar) and that sugar is necessary for proper brain functioning.  If you're buying into the hype about "sugar addiction" being bad for you, you may be doing something worse to yourself.

I discovered long ago, when doing various elimination diets to see if my problem was an undiagnosed food allergy, that in the weeks that I did without sugar, I couldn't think clearly.

Most (if not all) artificial sweeteners have their own health consequences.


5 reasons why you should consider blogging | Z-Blog

Sharing is caring
I am a whole-hearted advocate of the philosophy that knowledge is to be shared. Blogging can be a great platform for sharing what you've learned and know with others who may be interested in what you have to say and learn from you so they can improve their lives.

Tuesday, July 24, 2012

The cat that caught the mice

The cat that caught the mice

see cat that
caught the mice

Dr Coffin and Dr Pathak first voiced their opinion on the origin of XMRV
at CROI conference 2011 (1). Later they released a video (2) which
recounted how they had traced the birth of the virus to one cell line,
called 22Rv1, and how they had also miraculously identified two parental
viruses to XMRV (PreXMRV-1 and PreXMRV-2).  It was a fantastical tale
and had all the hallmarks of wondrous discovery that only the keenest
most focused minds could have identified, or at least this was the
impression many would have been given from the publicity surrounding the
paper, Paprotka et al. 2011 (3).

On further investigation the experiments in the paper, 'Recombinant
origin of the retrovirus XMRV' (3), could not have supported these
claims and the sequence uploaded into the GenBank which was said to have
come from the 22Rv1 cell line, and was named the "consensus" XMRV
sequence, did not include an env gene.  It had also been discovered that
XMRV was not the viruses that had been detected in the human population
by various scientists.  They were actually XMRV-like.

Earlier this week scientists from Germany published a study, Mayer et
al. 2012 (4), looking for one of the viruses which Paprotka et al. had
claimed was an ancestral virus to XMRV. Their research directly
contradicts what Paprotka et al. (3) and Cingoz et al. 2011 (5) had
proposed for the origin of this ancestral virus and the human XMRV-like

A short recap of Paprotka et al. (3) and Cingoz et al. (5). is provided
at the bottom of this article. The main points are given here in bullet
form as they relate to the German study.

No wild mice were screened in either paper.Only PCR was used in both
studies.45 Lab mice and 44 wild derived lab mice were negative for XMRV
in Paprotka et al.15 lab mice screened for PreXMRV-1 and -2 in Paprotka
(no wild derived lab mice). Several strains were positive.48 lab strains
and 46 wild derived lab strains were screened for PreXMRV-1 and -2 in
Cingoz et al. Several strains were positive.22Rv1 cell line created
using nude mice.So called PreXMRV-1 and -2 viruses found integrated into
hairy mice and not nude mice in Cingoz et al.PreXMRV-1 and PreXMRV-2
were claimed to be endogenous mouse viruses in Paprotka et al.


Virus Res. 2012 Jul 4. [Epub ahead of print]
Comparing PreXMRV-2 gag sequence diversity in laboratory and wild mice
using deep sequencing.
Mayer J, Mazzoni CJ, Greenwood AD.
Department of Human Genetics, Center of Human and Molecular Biology,
Medical Faculty, University of Saarland, 66421 Homburg, Germany.

It has recently been reported that the xenotropic murine leukemia
virus-related virus (XMRV) derives from a laboratory recombinant.
However, sequences with characteristics of the 5' half of XMRV (termed
PreXMRV-2) have been identified in several laboratory mouse genomes and
cell lines suggesting parts of the XMRV genome exist as naturally
occurring retroviruses in mice. We compare here PreXMRV-2 gag sequence
diversity in mice to that of reported XMRV-like sequences by testing a
panel of wild mouse and common inbred laboratory mouse strain genomic
DNAs and by using high throughput amplicon sequencing. Sequences with
features typical of previously reported PreXMRV-2 sequences, among them
a 24 nt deletion, were repeatedly identified in different wild mice and
inbred mouse strains within a high background of non-XMRV-like
sequences. However, Sanger sequencing of clones from amplicons failed to
retrieve such sequences effectively. Phylogenetic analysis suggests that
PreXMRV-2 gag sequences from mice, cell lines and patient samples belong
to the same evolutionarily young clade and that such sequences are
diverse and widespread within Mus musculus domesticus and laboratory
mice derived from this species. No evidence of PreXMRV-2 like gag
sequences could be obtained outside of the Mus musculus lineage. The
results suggest that accurate determination of presence, absence and
relationships of specific murine retroviral strains benefit greatly from
deep sequencing analysis.

Mayer et al. compared the diversity of PreXMRV-2 and XMRV-like sequences
in mice, both inbred strains and wild strains, and in a number of other
rodents, using both low throughput assays (PCR) and high throughput
assays (next generation sequencing).  In comparison to PCR, next
generation sequencing (NGS) produces millions more sequences of a virus.
Making it a far better approach for detecting low level infection by a
specific virus, than antiquated PCR techniques.  Surprisingly no study
had previously used NGS to chart the diversity of MLVs within mice or
using multiple individual mice.

According to the authors, the PreXMRV-2 virus was chosen as the
experiments could be constructed around the 24 nucleotide deletion in
the gag region of the virus. For those who are not aware, PreXMRV-2 is a
polytropic virus that is 99.9% similar in the gag and partial pol
regions to XMRV, which also has a 24 nucleotide deletion in its gag
region.  It is also important to note that the 67% positivity figure
from Lombardi et al. 2009 (6) was obtained using an assay targeting the
gag region of VP35, a virus with a high similarity (99.8%) in the gag
region to PreXMRV-2.  Of the two primer pairs used in this study the
second longer set are designed to detect the gag region of the VP35
human retrovirus.

Mayer et al. discovered that where NGS sequencing could detect MLV
viruses, PCR used in the Paprotka and Cingoz papers would generally
detect nothing.  Two reasons were suggested for this.  The low copy
number of the viruses and the partial deletion in the gag region of the
virus interfering with the specificity of the assays used.

The authors also highlighted how Cingoz et al. had claimed to have
identified XMRV-like sequences in various mice, but how they had
actually not attempted to sequence the products amplified by PCR, making
identification of the viruses merely an assumption.

Also, in contradiction to the findings of Paprotka and Cingoz using PCR,
Mayer et al. also found that when using NGS PreXMRV-2 has sequence
diversity in wild and inbred mice. This indicates that PreXMRV-2 cannot
be an endogenous mouse virus.

",human derived, cell line derived and mouse DNA derived XMRV-like
sequences showed poor tree structure, high diversity in the number of
lineages and did not cluster by DNA source…"

Their phylogenetic analysis also indicated that most of the sequences
containing the 24 nucleotide deletion from mice, cell line and human
tissue, as well as sequences without the deletion, were all derived from
an unknown clade, which contained a mix of polytropic and xenotropic
sequences.  Several sequences were similar but diverged from the
PreXMRV-2 virus after the 24 nucleotide deletion and were closer to
Xenotropic murine virus sequences.  An indication that these were
recombinant sequences combining PreXMRV-2 and a xenotropic virus.  A
common occurrence with viruses that have high recombination rates.  Due
to the high similarity of the sequences the clade was also thought to be
young.  In gamma retroviral terms this would be a few hundred years.

"The PreXMRV-2 virus likely originated recently in wild populations of
M. domesticus and may not be present in all populations."

From the mice tested they found that PreXMRV-2 likely originated in Mus
musculus domesticus (western European house mouse).  That several lab
mice and inbred lab strains were also infected.  Which would be
expected, as the majority of inbread lab mice are derived from M. m.
domesticus and some would inherit the PreXMRV-2 gag.

The authors also tested a museum sample of a wild mouse (M. m.
domesticus) captured in Ann Arbor Michigan, USA, in 1906.  The PCR
products from this sample were correct for this to be infected with a
virus from the PreXMRV-2 family clade, but due to the age of the sample
and subsequent degradation of the DNA they were unable to sequence.
Leading them to state that:

"we cannot conclude that PreXMRV-2 like sequences are absent in the
U.S. wild house mouse population. "

The authors suggest that PreXMRV-2 gag may be broadly present among
other various susbspecies of Mus musculus which they had not tested in
this study.

They concluded that the virus was not present at a high copy number in
mice and that consequently high-throughput (NGS) sequencing should
generally be employed when attempting to detect rare sequences of this
type.  NGS also being readily used for detecting rare HIV-1 variants.

The authors concluded that:

"The presence of a distinct clade including XMRV, PreXMRV-2, cell
line-derived and mouse DNA-derived sequences suggests that the 24 nt
deletion and gag specific features are shared due to common ancestry and
not due to independent generation of the deletion or other polymorphisms
within this group."

Again the main conclusions of the study are as follows:

PreXMRV-2 has diversity.  High-throughput sequencing will identify MLVs
which PCR cannot.PreXMRV-2 likely originated in M. m. domesticus.


This research is the final nail in the coffin for the lab contamination
story for the ME and prostate cancer retroviruses.  The viruses have not
been confined to the lab.  It is highly probably that recombination
events with PreXMRV-2 are occurring all the time in the wild, with both
other polytropic and xenotropic MLVs.  If anything this paper shows that
without full sequencing of the ME retroviruses and more prostate cancer
retroviruses, no claim can be made as to the variants and strains which
has been detected.

In addition, if MLVs cannot always be detected when using PCR, then how
can we expect researchers to correctly determine whether the same
viruses are infecting humans when they are using those inferior
techniques?  The negative studies are obsolete.

Much is not known about these viruses, but we now know that
high-thoughput sequencing needs to be a prerequisite in further studies
to uncover the truth.  Too much money and time has been lost chasing
viruses that can escape PCR detecting.


Paper # 91LB. Paprotka et al. 2011. XMRV Probably Originated through
Recombination between 2 Endogenous Murine Retroviruses during in vivo
Passage of a Human Prostate Cancer Xenograft. CROI.

NCI. 2011. Cancer Research Now: Investigating XMRV. Youtube.

Paprotka et al. 2011. Recombinant Origin of the Retrovirus XMRV.
Science. 333, 97-101.

Mayer et al. 2012. Comparing PreXMRV-2 gag sequence diversity in
laboratory and wild mice using deep sequencing. Virus Res.

Cingoz et al. 2012. Characterization, Mapping and Distribution of the
Two XMRV Parental Proviruses. JVI. DOI:10.1128/JVI.06022-11.

Lombardi et al. 2009. Detection of an Infectious Retrovirus, XMRV, in
Blood Cells of Patients with Chronic Fatigue Syndrome. Science. 326,


The claim in Paprotka was simple. A linear series of cells originally
from a prostate cancer patient which had been passed through mice had
been analyzed with various tests.  There were cells from early passages
and later passages through mice, and a third set of cells established
much later.  They could not find XMRV in the earlier cells, but could in
both of the later cells.  They also claimed that two endogenous viruses
(PreXMRV-1 and PreXMRV-2) were present in mice which in their words were
"likely to have been used" in creating the 22Rv1 cell line. Three
separate tests had been used to come to this conclusion.

The three tests were however used selectively on different cells and
mice, and each had a different limit of detection.  The first two tests
were in combination used on all items but the later cells that were
passed through mice.  Neither was ever established capable of detecting
XMRV at less than 2000 copies per 100 cells.  The third test being the
most sensitive type of the three tests was only used to then screen the
later cells that had been passed through mice, but no data was provided
on the sensitivity of this test (in fact the test is not even named in
the paper) and those cells in particular were never shown to have been
from the same patient as all other cells tested.

Of the mice that were screened there were no wild mice included, only
several strains of lab mice which had been derived from wild mice and a
number of lab mice strains.  None of the mice were those actually used
in the creation of the 22Rv1 cell line.

In summary the experiments within the study were not capable of
determining the origin of the virus was a single cell line.  The two so
called parental viruses were also not shown to be present for this
magical recombination to have occurred.  Finally the uploaded sequence
of the virus put into the NCBI database from the 22Rv1 cells was later
found to not include an envelop gene, and thus could not be claimed to
be the XMRV virus.

A later study from Dr Coffin (Cingoz et al. 2011), took the tale of the
two parental viruses further.  There he claimed that the viruses were
integrated into the genome of various lab mice, but the mice were not
nude mice which were those used for the creation of the 22Rv1 cell line.

15 July 2012

Monday, July 23, 2012

New light bulbs may be harmful to skin |

Just another reason I stocked up on incandescents so I wouldn't have to use CFLs in my house!

How Research Into Chronic Fatigue Syndrome Turned into an Ugly Fight


What happened there sounds like fiction: a scientific breakthrough, suspicion of contamination, a well-meaning scientist, a nonprofit institute, a fee-for-service diagnostic lab, and a legal battle that is still unfolding. In the process, Mikovits plunged from a leading light in the fight against a mysterious medical condition to an unemployed woman with a mark on her name in the world of science.

Sunday, July 22, 2012

Journalist Llewellyn King interviews Gunnar Gottschalk with Simmaron

Broadcast journalist Llewellyn King interviews Gunnar Gottschalk with
Simmaron Research.
"You can tell when people are sick and these people are incredibly sick."
Episode 30

People who wish to sponsor these ME/CFS alerts can contact the team at
* * *
So why can't DOCTORS see "these people are incredibly sick"?  Clearly, we are unwell, so why do they try to pin it on All In Your Head?