cars, car modify, diagnostic tools,cmd, remote cnt

growth policies no substitute for

2008-02-25T03:24:00.001-08:00

Growth policies: No substitute for thinking

economics sB growth sB policy sB

I have just finished reading Chapter 2 of Rodrik's latest book (which

is a revised version of this "Growth Diagnostics" paper):

Most well-trained economists would agree that the standard policy

reforms included in the Washington Consensus have the potential to

be growth-promoting. What the experience of the last 15 years has

shown, however, is that the impact of these reforms is heavily

dependent on circumstances...We argue in this paper that this calls

for an approach to reform that is much more contingent on the

economic environment, but one that also avoids an anything goes

attitude of nihilism. We show it is possible to develop a unified

framework for analyzing and formulating growth strategies that is

both operational and based on solid economic reasoning.

The authors then offer a growth diagnostics framework that is

summarized by Rodrik here. The paper concludes with the following:

Across-the-board reform packages have often failed to get countries

growing again. The method for growth diagnostics we provide in this

paper should help target reform on the most binding constraints

that impede growth... As our discussion of El Salvador, Brazil, and

the Dominican Republic illustrates, each of these circumstances

throws out different diagnostic signals. An approach to development

that determines the action agenda on the basis of these signals is

likely to be considerably more effective than a laundry-list

approach with a long list of institutional and governance reforms

that may or may not be well targeted on the most binding

constraints to growth.

I agree with Rodrik's general message on the context-dependency of

growth policies. His offered framework is also useful for

policymakers. Yet it is no substitute for thinking by developing

countries' economists and policymakers: They need to analyze which of

the agenda are particularly relevant to their respective economies.

Rodrik puts it best: "The framework does not economize on inputs (the

thoughtfulness required to reach decisions), only on outputs (the list

of things that we recommend governments should do to get growth

going)".

PS: For a somewhat similar exercise for Indonesia (though it doesn't

seem to be using this exact framework), see the reports posted here

(particularly its Special Focus on Regions reports, on the left

sidebar).

PPS: Here is a set of papers commissioned by the Commission on Growth

and Development.

PPPS: Charles Kenny offers a review of new evidence on growth in the

last six years (his answer: Not very much!). HT: Marginal Revolution.

Labels: development, economics, growth, policy

posted by Arya Gaduh at 10:42 AM

0 Comments:

health insurance for poor

2008-02-25T03:14:00.001-08:00

Health Insurance for the Poor

As a result of personal endeavors that seek to bridge the inequality

in healthcare, I was recently perusing the web and came across some

interesting organizations that are providing health insurance to the

rural poor in India. With less than 2% of India's 700 million rural

poor insured, there is a huge unmet need. I was pleasantly surprised

to find no less than 25 "Microfinance"-like Health Insurance schemes

and will attempt to highlight a few of the main players here:

Yeshaswini Co-operative Health Insurance Scheme was started in 2003 in

rural Karnataka. The program originated in the mind of Dr. Devi

Shetty, a very wealthy cardiac surgeon and philanthropist who

pioneered the spread of telemedicine as well as low cost cardiac

operations in India. In addition to his for-profit operations, Dr.

Shetty runs a not-for-profit hospital, Narayana Hrudayalaya, in

Bangalore.

Yeshaswini aimed to create a large insurance scheme, where the law of

large numbers would overcome the risk of an unexpectedly large number

of enrollees making claims in the first year, which had caused the

financing problems associated with the small schemes of the past. The

plan for the Yeshaswini Health Insurance Scheme, was very low premiums

with a very large number of participants.

The Scheme covers the farmer co-operator, his spouse and children. The

premium contributed per person was Rs 5 per month with Rs 2.5 subsidy

from the government of Karnataka in the first year. The Yeshasvini

beneficiary is entitled to the following benefits: free outpatient

services at a network hospital including consultation fee and

registration fee, investigation at special discounted rates, over 1600

listed surgeries done free of cost at network hospitals.

The following charges are covered for any of the surgeries included in

the policy: Admission, bed, nursing, anaesthesia, OT, surgeons, cost

of consumables and medicines during the surgery and post operative

period, surgery-related post and pre-operative investigations. The

surgical cover is 100 per cent cashless. 16 lakh farmers had enrolled

as members in the first year, 35000 members availed of free

consultation at network hospitals, 9039 surgeries were done cashless

amounting to Rs 10.53 crores; of these 657 were cardiac surgeries. In

the second year, 22 lakh farmers became members of the Scheme of which

82652 members have availed of free outpatient consultation. More than

23000 surgeries have been conducted free of cost.

A good case study of Yeshaswini is available here

Healing Fields Health Insurance Scheme

Members pay Rs 285 ($5 per year;0.003 - less than a cent per day per

family member!) annually to cover health insurance (Rs 20,000) for a

family of five and Rs 35 for Personal Accident Benefit (Rs 25,000 each

on member and spouse) to HDFC Chubb, the insurance company for the

scheme. The policy is low-cost, which includes pregnancy and covers 43

listed common illnesses governed by `Diagnostic Related Group (DRG)

Model'. In case of a hospitalisation, up to 25 percent is paid by the

patient as co-payment. The stakeholders, insurer, NGO partner and the

hospital together work out a customised process, map and goals, for

the success of the scheme.

Arogya Raksha Yojana is a year old and offers: Free out patient

consultation, generic medicines at special rates from network hospital

pharmacies and Biocare pharmacies, diagnostic tests at discounted

rates at network hospitals and approved diagnostic centres,

hospitalisation not leading to surgery, surgical treatment for over

1600 types of surgeries, 100% cashless facility for surgical treatment

new logging experience

2008-02-25T02:59:00.001-08:00

A new logging experience!

I've been using logback for a few months now, and I'm impressed!

With excellent documentation and support, neat logging features,

blazing performance and an innovating eclipse plugin, I've finally

found a good replacement for the good old log4j.

The first thing I really appreciate compared to log4j or the java

logging api is the documentation. The guide is well written, they have

a nice demo, and you are up to speed in a few minutes.

Neat logging features

There are some very simple features which makes the life so much

easier, such as the intelligent logger name reduction when it's too

long: instead of simply truncating the name, it put the first letter

of each package:

09:59:04.203 [main] INFO o.x.x.web.XoosentApplication - starting XooSent

The Mapped Diagnostic Context (MDC) is also a killing feature. It

allows to associate metadata to the current thread, to correlate

messages to their context. For instance in a web application with

authentication, you can associate the user name to the the thread and

add this user name to all log messages, without any change to your log

calls. For instance, you add this at user authentication time:

MDC.put("user", username);

Then in your logback configuration you can use %Xuser in your pattern,

and you will see the authenticated user name. It's that simple, and in

multithreaded environment where multiple traces overlap, it really

helps.

Updated: As Jorg pointed out, this isn't a feature introduced by

logback, as log4j already supports NDC and MDC.

Performance

The parametrized logging is a key feature of logback, which improves

performance by avoiding a toString() call when your message is not

logged:

logger.debug("Hello, my name is {}, I am {} years old", username, age);

Note that obviously the performance gain applies only if you don't

enclose your logging statements with if (logger.isDebugEnabled())

statements). But if you look at a benchmark run by Sebastien Pennec,

one the developers of logback, it's really impressive:

Log4j direct debug call: 442

Log4j tested (isDebugEnabled) debug call: 19

Logback direct debug call: 435

Logback tested (isDebugEnabled) debug call: 10

Logback parametrized debug call: 15

OK, we all know how we should consider benchmarks, especially when

written by someone biased as Sebastien obviously is, but these numbers

can't be completly wrong, and what's interesting is that a logback

parametrized call takes approximately the same time as a log4j

isDebugEnabled call. Really cool!

Still on the performance area, logback introduces TurboFilters, which

allows to filter logging before the logging event is actually

constructed, saving a lot of unnecessary time.

Beyond console and files

Beyond classical ways to track and configure your logs, you have very

interesting features with logback, such as a JMX configuration, and a

new Eclipse plugin which is really neat.

One of the thing I like the most with this plugin is the option to go

to the source which is at the origin of the log. Double click on the

log, and it will open your source editor at the line where the log

call is performed! Awesome! How many times did I use the search tool

to find where a particular log call is performed in a big application,

and waste time because the message was the result of a concatenation

and thus my search failed...

Another interesting thing is the option to change the pattern and

apply it to all the logs, including previous one.

And you have also a good filter option, where you can apply any

logback filter expressions. This still need to be improved IMO to be

able to apply the filter in real time to previous logs, but hey, it's

only the first version of this plugin!

Excellent support

Last but not least the support is amazing. There isn't much traffic on

the user mailing list for the moment (their documentation is so good

:-)), but very often developers take time to answer your questions

with a lot of details, trying to reproduce your environment, and

single gene controls emotional recall

2008-02-25T02:54:00.001-08:00

A Single Gene Controls Emotional Recall!

And the neurotransmitter norepinephrine (NE), which has been in the

news lately, plays a key role in the overstated headline of the day:

Emotional recall is in your genes

18:00 29 July 2007

Paul Marks

Image from Fig. 1A of Depue et al. (2007)

Your ability to recall emotional events - such as meeting the love

of your life, or the trauma of a painful car crash - is governed by

a common variation in a single gene, according to a new study.

[NOTE: As if variations in many other genes were tested.]

. . .

Highly emotive incidents trigger the brain to release the hormone

and neurotransmitter noradrenaline. This stimulates the amygdala -

part of the brain involved with processing emotional reactions - to

store memories in the hippocampus and other parts of the brain,

says Dominique de Quervain, a neuroscientist at the University of

Zurich in Switzerland.

Yet for some reason, recall of emotional events varies a great deal

from person to person. So de Quervain wondered if common variations

in a gene called ADRA2B, which codes for [one of the subtypes of

the alpha-2] noradrenaline receptor, could be responsible. Some 30

per cent of Caucasians and 12 per cent of Africans possess this

variant, he says.

So this is the alpha-2 receptor, which responds to clonidine (agonist)

and yohimbine (antagonist), rather than the beta-2 receptor, which is

antagonized by our old friend, propranolol. According to the NCBI

Sequence Viewer v2.0 Summary on ADRA2B adrenergic, alpha-2B-, receptor

[Homo sapiens]:

Alpha-2-adrenergic receptors are members of the G protein-coupled

receptor superfamily. They include 3 highly homologous subtypes:

alpha2A, alpha2B, and alpha2C. These receptors have a critical role

in regulating neurotransmitter release from sympathetic nerves and

from adrenergic neurons in the central nervous system. This gene

encodes the alpha2B subtype, which was observed to associate with

eIF-2B, a guanine nucleotide exchange protein that functions in

regulation of translation. A polymorphic variant of the alpha2B

subtype, which lacks 3 glutamic acids from a glutamic acid repeat

element, was identified to have decreased G protein-coupled

receptor kinase-mediated phosphorylation and desensitization; this

polymorphic form is also associated with reduced basal metabolic

rate in obese subjects and may therefore contribute to the

pathogenesis of obesity. This gene contains no introns in either

its coding or untranslated sequences.

Let's return to the New Scientist article.

One group comprised healthy Swiss citizens and the other comprised

traumatised survivors of the Rwandan genocide - who were living in

a refugee camp in Uganda.

The researchers found that, in both groups, people carrying the

ADRA2B gene variant were "substantially more likely" to remember

both positive and negative pictures than people with other forms of

the gene. Neutral images were recalled to the same degree by people

with and without the variant.

However, Rwandans with the variant had far higher recall of

negative emotional events than the Europeans who carried it - and

this was unrelated to whether or not they suffered from post

traumatic stress disorder.

"The genetic variant is related to enhanced emotional memory,"

concludes de Quervain. "But it also appears to predispose people to

stronger traumatic memories when something terrible happens."

Is that the same as saying that a single gene governs your ability to

recall emotional events? It certainly appears to influence one's

ability to recall emotional events, whether pleasant, unpleasant, or

traumatic. That's not to say, however, that other genes do not have

any influence over such complicated cognitive and affective processes.

In the paper (de Quervain et al., 2007), a large group of normal Swiss

participants (n=435) was shown a series of photographs from the

International Affective Picture Set (10 each positive, negative, and

neutral in emotional content) and asked to rate them on valence and

arousal. Ten minutes later, they were asked to recall the words.

Overall, the participants showed an advantage in recalling emotional

words relative to neutral words: 57% better for positive and 55% for

negative. The breakdown for carriers and noncarriers of the variant

are shown in the table below, which illustrates that the carriers

showed a significantly greater enhancement in emotional recall.

SWISS

All emotional pictures

carriers (N = 214) 78% +/- 7%

noncarriers (N = 221) 43% +/- 6%

Positive

carriers 77% +/- 8%

noncarriers 43% +/- 7%

Negative

carriers 79% +/- 7%

noncarriers 43% +/- 6%

The second group of participants had survived one of the most horrific

events of the 20th century: the 1994 genocide of 1,000,000 human

beings in Rwanda over the course of only 100 days (Survivors Fund,

SURF). These individuals were in a refugee camp and were recruited to

participate not in the trivial picture recall task, but to report

their experiences in a clinical setting. At this point, it's best to

quote the paper directly:

We hypothesized that deletion carriers would have increased

emotional memory for traumatic events reflected in increased

re-experiencing symptoms. We tested this hypothesis in 202 refugees

who had fled from the Rwandan civil war and were living in the

Nakivale refugee camp in Uganda at the time of investigation (100

females, 102 males; median age, 34 years...). All subjects had

experienced multiple, highly aversive situations and were examined

by trained experts with a structured interview based on the

Post-traumatic Diagnostic Scale with the help of trained

interviewers chosen from the refugee community. Traumatic events

were assessed using a checklist of 31 war- and nonwar-related

traumatic-event types (for example, injury by a weapon, rape,

accidents). The population consisted of 133 subjects fulfilling the

diagnostic criteria of DSM-IV for post-traumatic stress disorder

(PTSD) and 69 subjects without PTSD or a history of PTSD. Deletion

carriers had a significantly higher score for re-experiencing

symptoms per traumatic-event type than did noncarriers (carriers,

N=42, 0.47 +/- 0.05; noncarriers, N=160, 0.31 +/- 0.03), whereas

the deletion was not significantly associated with hyperarousal or

avoidance symptoms. The association of the deletion with increased

traumatic memory was independent of the presence of PTSD ... and

the genotype was equally distributed across the diagnostic groups.

Correcting for gender did not influence the genotype effect on

traumatic memory.

Fig. 3 (de Quervain et al., 2007)

The authors' conclusion:

Taken together, we show that a genetically anchored alteration in

the noradrenergic system is related to enhanced emotional memory in

healthy young Swiss subjects. Furthermore, we found that the same

genetic alteration is related to increased traumatic memory in a

Sub-Saharan African population of civil war refugees who

experienced multiple and highly aversive emotional situations. The

present findings suggest that the price for the deletion-related

enhancement of emotional memory may be enhanced intrusive and

distressing emotional memory for traumatic events.

Reference

de Quervain DJ, Kolassa IT, Ertl V, Onyut PL, Neuner F, Elbert T,

Papassotiropoulos A. (2007). A deletion variant of the alpha

2b-adrenoceptor is related to emotional memory in Europeans and

Africans. Nature Neurosci. Published online: 29 July 2007.

Emotionally arousing events are recalled better than neutral events.

This phenomenon, which helps us to remember important and potentially

vital information, depends on the activation of noradrenergic

transmission in the brain. Here we show that a deletion variant of

ADRA2B, the gene encoding the alpha2b-adrenergic receptor, is related

to enhanced emotional memory in healthy Swiss subjects and in

survivors of the Rwandan civil war who experienced highly aversive

emotional situations.

Symbol Report: ADRA2B

posted by The Neurocritic @ 3:42 PM 0 comments links to this post

0 Comments:

2005_06_01_archive

2008-02-25T02:44:00.001-08:00

Concept Hierarchy

http://profusion.bu.edu/techlab/Docs/Tan__Concept_Hierarchy_Memory_Mod

el.pdf

Eclipse plugin install:

Plugin install for eclipse is get the zip and install it in the

directory of plugins and directory of features

Eclipse

1. plugins

2. features

Extract the files into these directories.

-Kalyan

Posted by kalyan at 5:09 PM 0 comments

Request Tracker Biggest Issue

The request tracker ticket creation is a big pain, I think i was able

to solve the ticket creation issue but it has cropped up again ...

since i forgot what i did to resolve it ( some permission problem)

need to look and document it..

Things which i have tried and which does not work

1. User and group setting in web apache server ( www and other , kosh

2007_07_01_archive

2008-02-25T02:34:00.001-08:00

Renal-hepatic-pancreatic dysplasia syndrome (ivemark's syndrome) with

lymphangiectasia

Renal-hepatic-pancreatic dysplasia syndrome (ivemark's syndrome).

With lymphangiectasia as a complication

Diagn Pathol. 2007 Jul

Vankalakunti M, Gupta K, Kakkar N, Das A.

ABSTRACT

BACKGROUND: Renal-Hepatic-Pancreatic dysplasia syndrome described by

Ivemark in 1959 constitutes a triad pancreatic fibrosis, renal

dysplasia and hepatic dysgenesis.

CASE PRESENTATION: We describe two unrelated cases of

Renal-hepatic-pancreatic dysplasia syndrome in stillborn babies. The

characteristic microscopic features were present in both the cases.

The second case illustrates the unique association lymphangiectasia

with Renal-hepatic-pancreatic dysplasia syndrome. Both cases are

unrelated and there is no history of any consanguineous marriage.

CONCLUSION: These two cases are unrelated and are rare. In the

developmental research, the perinatal autopsy needs to be utilized as

a major tool and an Ad hoc committee formation is required to

formulate the approach towards syndromic diseases.

Diagnostic Pathology

lecturer in veterinary pathology

2008-02-25T02:24:00.001-08:00

diagnostic imaging for tinnitus

2008-02-25T02:14:00.001-08:00

Diagnostic imaging for Tinnitus

Magnetic resonance angiography or venography (MRA and MRV) can be used

to evaluate malformations of the blood vessels. Computed tomography

scans (CT scans) or magnetic resonance imaging scans (MRIs) can be

used to locate tumors or abnormalities of the brain stem.Blood tests

The doctor may order a complete blood count (CBC) with specific

on belay belay on

2008-02-25T01:59:00.001-08:00

THE_URL:http://centennialsl5e2j.blogspot.com/2008/02/on-belay-belay-on.html

THE_TITLE:Blogger: 404 Error - Page not found.

Blogger

Push-Button Publishing

Page Not Found

The requested URL was not found on this server. Please visit the

Blogger homepage or the Blogger Knowledge Base for further assistance.

you have entered twilight zone

2008-02-25T01:54:00.001-08:00

you have entered: the twilight zone

So the people at the pharmacy think I have lost my mind, but it is not

I. Somebody, but not I.

Last month they told Lance that the Clomid would have been covered by

my insurance if only the doctor had precertified it. "No it wouldn't,"

I said when he came home. Our insurance does not cover infertility

treatment. At all. Believe me, the experience of finding this out was

so harrowing that the fact is now permanently engraved in my skin.

Lance wasn't sure, but thought the pharmacy had actually been told

this by my insurance when they called to put the prescription through.

He persuaded me it didn't hurt to try.

So this month I tried. Called the doctor's office and asked them to

precertify it.

Wouldn't you know, the doctor's office called right back (after I

waited 24 hours and called them again, I mean) and said my insurance

told them it doesn't NEED to be precertified. It's just covered.

Now me, I am not an idiot. I've been through this before. I know my

insurance sows misinformation like the plague. I know that if three

different people call, my insurance will give them three different

answers (maybe they cycle through them, or something?), but I KNOW

infertility medications are not covered on my plan. I call them

myself.

"Your insurance does not cover medications prescribed for the

treatment of infertility." Thank you. I knew that. So the information

the other representative gave my doctor's office was incorrect. "No.

Because if you had one of our plans that did cover infertility

medication, it would not need to be precertified."

Ah. So you figured, when my doctor called about me, she was asking

about a plan some other people have, not the one *I* have? Oh, forget

it.

Several hours and a lot of muttering under my breath about the waste

of time this was later, I'm off to the pharmacy. Instead of the $65

total I'm expecting, the clerk tells me I have a $10 copay. I stare at

her blankly, and then say "Are you sure?" She says it went through; my

insurance okayed it. I tell her it's a mistake. She calls over the guy

in charge. What's your problem, he wants to know? No one's going to

bill you. Your insurance okayed it. What did you do last month? We

paid up front, I say. He goes to look. No, your insurance covered it

last time, too.

OK, what??

Now I'm home, I know I didn't imagine that part. There's a charge for

$65 on our visa statement. But with all those people looking at me

like I was crazy in the head, I couldn't express what I was worried

about, exactly. I guess, uh, what difference DOES it make if I pay now

or get billed later? So I let them goad me into doing it. I paid the

copay and went home.

I think what the guy in charge was trying to say, without outright

saying it, was that if my insurance made a mistake and let it go

through, they're not likely to catch it. On the way home I wondered if

this felt dishonest. I decided it wasn't. After all, if my insurance

tells everyone who calls something different, who's to say they're

lying to them and not to me? Maybe I have fabulous infertility

coverage and just don't know it.

I don't, though. We're going to get a bill. Count on it. And the next

time my insurance lies, I will have to take the bait all over again.

Because what if it's the one time they're telling the truth, and it

job opportunities at quest diagnostics

2008-02-25T01:44:00.001-08:00

early diagnosis of prostate cancer

2008-02-25T01:14:00.001-08:00

Early Diagnosis Of Prostate Cancer

Treating prostate cancer is a race against time. By the time the

patient can feel the first symptoms, the disease has usually spread

too far. A novel diagnostic technique combines optical imaging with

ultrasound, thus improving early diagnosis.

By the time the first symptoms of prostate cancer become apparent, the

tumor has usually spread too far and there is little hope of curing

it. Early diagnosis can help to save lives. While CAT scans, X-rays

and magnetic resonance devices can frequently detect tumors in time,

the cost of routine examinations is often too high, and the devices

are not always sensitive enough. Ultrasound is a cost-efficient

alternative, but is not very reliable.

A novel, cost-efficient and sensitive device will soon increase the

number of early diagnoses of prostate cancer and offer more patients

the prospect of recovery. This diagnostic device was developed by

researchers at the Fraunhofer Institute for Biomedical Technology IBMT

in St. Ingbert in collaboration with partners from five European

countries. The European Commission is funding the project to the tune

of 2.2 million euros. "We use a combination of two different imaging

techniques: optical imaging and ultrasound," says IBMT department

manager Dr. Robert Lemor. "We shine laser light into the tissue,

causing it to heat up and expand. This generates pressure in the form

of a sound wave, which spreads through the tissue in much the same way

as ultrasound and is also detected in the same way." The researchers

thus combine the good contrast of light with the good spatial

resolution of sound, using the advantages of both systems.

In order to detect cancer cells at an early stage, however, the

researchers require an even stronger contrast between cancerous and

healthy cells. "We achieve this by using gold particles just a few

nanometers in size. Gold absorbs the laser's infrared light much

better than the cells, and therefore appears brighter in the picture,"

says Lemor. The researchers attach antibodies to the gold particles,

and these antibodies bond with specific proteins. These occur several

thousand times more frequently in cancer cells than in healthy tissue.

"This means that the gold accumulates specifically around the cancer

cells, while hardly any gold is found on healthy cells," explains

Lemor. The gold particles not only serve diagnostic purposes but can

also be used for therapy. If the laser output is increased and the

tissue is irradiated for a longer period, the gold heats up and the

generated heat destroys the cancer cells. Healthy tissue is not

affected, as hardly any gold accumulates in it. The researchers will

present the prototype of this diagnostic and therapeutic device at the

Medica trade fair (Hall 10, Stand F05) in D�sseldorf from November 14

to 17. If all goes well, says Lemor, the clinical study could begin in

about two to three years.

Get great free widgets at Widgetbox!

small beautiful guj_20

2008-02-25T00:59:00.001-08:00

2006_04_01_archive

2008-02-24T23:59:00.001-08:00

Changing careers...not just jobs!!!

I really do believe a lot of people never really find their "career

calling." It's never too late to change careers! Yes, it may take some

additional sacrifices and education to excel in your new career

choice, but if your current path does not have passion, then it might

be time to make a CAREER change. The next problem is deciding out what

you want to do. If you are reading this and would like to find out

what other types of jobs are out there, I may have some help. If you

have children who need some career path information, this information

is very valuable.

The US Government has a website that breaks down 1,000's of careers in

detail. Please visit http://www.bls.gov/oco/. Here you will find

fantastic information about potential career paths. Here is a sampling

of careers they profile along with earning potential.

Diagnostic Medical Sonographers http://www.bls.gov/oco/ocos273.htm

Diagnostic imaging embraces several procedures that aid in diagnosing

ailments. Besides the familiar x-ray, another common diagnostic

imaging method is magnetic resonance imaging, which uses giant magnets

that create radio waves, rather than radiation, to form an image. Not

all imaging technologies use ionizing radiation or radio waves,

however. Sonography, or ultrasonography, is the use of sound waves to

generate an image for the assessment and diagnosis of various medical

conditions. Sonography usually is associated with obstetrics and the

use of ultrasound imaging during pregnancy, but this technology has

many other applications in the diagnosis and treatment of medical

conditions.

Median annual earnings of diagnostic medical sonographers were $52,490

in May 2004. The middle 50 percent earned between $44,720 and $61,360

a year. The lowest 10 percent earned less than $37,800, and the

highest 10 percent earned more than $72,230. Median annual earnings of

diagnostic medical sonographers in May 2004 were $53,790 in offices of

physicians and $51,860 in general medical and surgical hospitals.

Geoscientists http://www.bls.gov/oco/ocos288.htm

Geoscientists study the composition, structure, and other physical

aspects of the Earth. With the use of sophisticated instruments and by

analyzing the composition of the earth and water, geoscientists study

the Earth's geologic past and present. Many geoscientists are involved

in searching for adequate supplies of natural resources such as

groundwater, metals, and petroleum, while others work closely with

environmental and other scientists in preserving and cleaning up the

environment.

Median annual earnings of geoscientists were $68,730 in May 2004. The

middle 50 percent earned between $49,260 and $98,380; the lowest 10

percent earned less than $37,700, the highest 10 percent more than

$130,750.

Boilermakers http://www.bls.gov/oco/ocos221.htm

Boilermakers and boilermaker mechanics make, install, and repair

boilers, vats, and other large vessels that hold liquids and gases.

Boilers supply steam to drive huge turbines in electric powerplants

and to provide heat and power in buildings, factories, and ships.

Tanks and vats are used to process and store chemicals, oil, beer, and

hundreds of other products.

In May 2004, the median hourly earnings of boilermakers were about

$21.68. The middle 50 percent earned between $17.80 and $26.82. The

lowest 10 percent earned less than $14.07, and the highest 10 percent

earned more than $32.46. Apprentices generally start at about half of

journey-level wages, with wages gradually increasing to the journey

epidemic never was

2008-02-24T23:44:00.001-08:00

Epidemic never was

New Scientist magazine

The Autism Epidemic that Never Was

RICHARD Miles will never forget the winter of 1989. The 34-year-old

company director and his family spent that Christmas on the island of

Jersey in the English Channel, where he had grown up. It was also then

that he first noticed something was badly wrong with his 14-month-old

son Robert. The bright, sociable child, who had already started

talking, became drowsy and unsteady on his feet. Then he started

bumping into furniture. Within weeks his language had dried up and he

would no longer make eye contact. "It was as if the lights went out,"

says Miles. His son was eventually diagnosed with autism.

Miles, who now campaigns for more research into autism, is convinced

that his son is part of an autism epidemic. Ten years ago, he points

out, Jersey had just three autistic children in special-needs

education. It now has 69. Robert was one of a cluster of nine children

on the island diagnosed around the same time.

Similar rises have been reported across the world, from Australia to

the US, and from Denmark to China. Back in the 1970s, specialists

would typically see four or five cases of autism in a population of

10,000. Today they routinely find 40, 50 or even 60 cases. Perhaps the

starkest illustration of autism's relentless rise comes from

California. In 2003, the state authorities stunned the world when they

announced that over the previous 16 years, the number of people

receiving health or education services for autism had risen more than

sixfold. The world's media went into overdrive.

What could be causing so many children to lose their footing on a

normal developmental trajectory and crash-land into the nightmare

world of autism? The change has occurred too suddenly to be genetic in

origin, which points to some environmental factor. But what? There is

no shortage of suspects. In the UK, blame is often laid at the door of

the combined measles, mumps and rubella (MMR) vaccine. In the US,

mercury added to a range of childhood shots has been accused. Food

allergies, viral infections, antibiotics and other prescription drugs

have all been fingered, often by campaign groups run by mystified and

angry parents. The problem is that none of these suggested causes has

any solid scientific evidence to support it (see "The usual

suspects").

Perhaps there's a simple explanation for this: there is no autism

epidemic. On the face of it that sounds ridiculous - just look at the

figures. But talk to almost any autism researcher and they will point

to other explanations for the rise in numbers. Some say it's still an

open question, but others are adamant that the autism epidemic is a

complete myth. And if the most recent research is anything to go by,

they could be right. Studies designed to track the supposedly

increasing prevalence of autism are coming to the conclusion that, in

actual fact, there is no increase at all. "There is no epidemic," says

Brent Taylor, professor of community child health at University

College London.

Autism is a developmental disorder sometimes noticeable from a few

months of age but not usually diagnosed until a child is 3 or 4 years

old. It is characterised by communication problems, difficulty in

socialising and a lack of imagination (see "What is autism"). It is

not a single disorder, but comes in many forms, which merge into other

disorders and eventually into "normality". There is no biochemical or

genetic test, so diagnosis has to be made by observing behaviour.

Autistic children also often have other medical conditions, such as

hyperactivity, Tourette's syndrome, anxiety and depression. The upshot

is that "one person's autism is not another person's autism," says

epidemiologist Jim Gurney of the University of Minnesota in

Minneapolis.

In recognition of this ambiguity, autism is considered part of a

continuum within a broader class of so-called "pervasive developmental

disorders" (PDDs) - basically any serious abnormality in a child's

development. Autism itself is divided into three categories: autistic

disorder, Asperger's syndrome (sometimes called "high-functioning

autism"), and pervasive developmental disorder-not otherwise specified

(PDD-NOS), sometimes called mild or atypical autism. Together these

three make up the autistic spectrum disorders.

"Californian authorities stunned the world when they announced a

sixfold rise in autism over the past 16 years"

Confused? You're not the only one. The difficulty of placing children

with developmental problems on this spectrum has led to several major

shifts in the way autism is diagnosed in the past 30 years. In the

late 1970s, the autism label was kept for those with severe problems

such as "gross language deficits" and "pervasive lack of

responsiveness". But since 1980 the diagnostic criteria have been

revised five times, including the addition of PDD-NOS in 1987 and

Asperger's in 1994.

This massive broadening of the definition of autism, particularly at

the milder end of the spectrum, is one of the main factors responsible

for the rise in cases, says Eric Fombonne of McGill University in

Montreal, Canada, a long-standing sceptic of the epidemic hypothesis.

Tellingly, around three-quarters of all diagnoses of autism today are

for Asperger's and PDD-NOS, both of which are much less severe than

the autism of old. "There is no litmus test for who is autistic and

who is not," says Tony Charman of the Institute of Child Health at

University College London.

Changes in diagnostic criteria apart, there are other reasons to

believe that autism is simply being diagnosed more often now than in

the past. One is the "Rain Man effect" - the huge increase in the

public awareness of autism following the 1988 film starring Dustin

Hoffman. Awareness has also increased massively among healthcare

workers. "Twenty years ago there were maybe 10 autism specialists in

the country. Now there are over 2000," says Taylor.

Another factor is that one of the stigmas of autism has largely

disappeared. Until about 10 years ago a prominent idea was that autism

was caused by an unloving "refrigerator mother". Now it is a no-blame

disease. "Parents are more willing to accept the label," says Taylor.

One expert New Scientist spoke to went as far as to describe autism as

"trendy".

Finally, while some parents still have to fight for help for their

autistic children, far more services are now available. This has

encouraged doctors to label borderline or ambiguous cases as autism -

they know this is often the best way to get the child some help. It

also makes autism an attractive diagnosis for parents. "I hear stories

of parents who are anxious to get a particular diagnosis if that is

what is required to obtain the services their child needs," says

Sydney Pettygrove, a paediatrician at the Arizona Health Sciences

Center in Tucson. In the UK, says Simon Baron-Cohen of the Autism

Research Centre at the University of Cambridge, "in every town there

are trained clinicians who can make a diagnosis."

It is hard to quantify these trends, but many epidemiologists now

believe that they can account for the apparent rise in autism the

general public and media take for granted. Proving it, however, is

difficult - if not impossible. The main problem is that an

epidemiological study carried out in the 1980s simply cannot be

compared with one done last week. There will be so many differences in

diagnostic procedures and in the willingness of doctors and parents to

label a child autistic that comparisons are meaningless. "You can't

control for everything," says Charman.

And so attention has shifted to what epidemiologists sniffily refer to

as "service provider data", such as the California figures. Ever since

1973, the authorities there have been keeping records of the number of

people receiving some kind of state help in connection with autism. In

2003, California's Department of Developmental Services (DDS)

announced a chilling figure that captured the world's attention. In

the 16 years to 2002, cases rose from 2778 to 20,377 (see Graph).

Among autism campaigners these figures are often cited as

incontrovertible and final proof of the existence of the autism

epidemic.

But there are serious problems with this interpretation. First, the

figures are raw numbers from public services, not a proper

epidemiological study. Critics point out they are not corrected for

changes in diagnostic criteria or for the growing awareness of autism.

"Prisons and institutions could be full of autistic adults labouring

under wrong diagnoses such as schizophrenia"

There is evidence, for example, that as the California autism numbers

have risen, diagnoses of mental retardation have fallen. Researchers

at Boston University School of Medicine in Massachusetts have found a

similar pattern in the UK. This effect, dubbed "diagnostic

substitution", cannot explain all the increase but is one example of

how diagnostic fashions can skew the data.

Another potential flaw is that the California figures don't take into

account the fact that the state's population is growing rapidly.

Between 1987 and 1999, the total population rose by nearly 20 per

cent, and the age group 0 to 14 rose even more steeply, by 26 per

cent.

As a result of these doubts and unknowns in the California figures,

most epidemiologists refuse to draw firm conclusions from them. "The

report doesn't change anything," says Charman. "It's not a systematic

study." In fact, the preface of the most recent California report

contains a health warning not to read too much into the numbers. "The

information should not be used to draw scientifically valid

conclusions," it says.

Some researchers, notably Robert Byrd of the MIND Institute at the

University of California, Davis, have attempted to correct for all the

unknowns. In an analysis published on the state DDS website nearly

three years ago, Byrd concluded that the rise is real. "Autism rates

are increasing," he told New Scientist. Some scientists accept that

Byrd's analysis lays to rest the idea that population growth could

have significantly swelled the figures. But his methods for

investigating the other potential sources of bias have been heavily

criticised, and tellingly, Byrd has not yet succeeded in getting his

study published in a peer-reviewed journal. Until he does, it is hard

to know how much weight to give his conclusions.

Perhaps the strongest case against the "better diagnosis" theory is

that, if true, there should be a "hidden hoard" of autistic adults who

were never properly diagnosed in childhood. To parent Richard Miles,

this is compelling. "My doctor cannot believe that he could have

missed so many cases in the past," he says. But Taylor disagrees. As a

former general practitioner, he says there are many children today

diagnosed with autism who would not have been labelled as such in the

past.

This view is difficult to substantiate, but in 2001 a team led by

Helen Heussler of Nottingham University, UK, had a crack. They

re-examined the data from a 1970 survey of 13,135 British children.

The original survey found just five autistic children, but using

modern diagnostic criteria Heussler's team found a hidden hoard of 56.

That's over a tenfold rise in numbers, which puts the California

figures in perspective. Heussler and her colleagues concluded that

"estimates from the early 1970s may have seriously underestimated the

prevalence".

Lorna Wing, a veteran autism researcher at the Institute of Psychiatry

in London, agrees. In the 1970s she spent a lot of time working with

special-needs children in the London district of Camberwell. Wing

reckons that at the time, fewer than 10 per cent of autistic children

were correctly diagnosed. She also thinks that prisons and

institutions are full of autistic adults labouring under wrong

diagnoses such as treatment-resistant schizophrenia or ADHD.

Ultimately, however, it may be impossible to tell whether there has

been a genuine rise in the incidence of autism over the past 30 years.

"There is no clear evidence that there has been an increase, but

there's no proof that there hasn't," says Charman. Even the

arch-sceptic Fombonne accepts this. "We must entertain the

possibility," he says. "But we don't have the evidence."

But researchers can answer another question: is the incidence of

autism continuing to rise? There is a tried and tested method of

tackling this sort of question. You carry out a large prevalence study

among a particular age group, and then repeat it a few years later

with a new set of individuals, in the same place and using exactly the

same methods. Several such studies into autism are ongoing, notably

one funded by the US Centers for Disease Control and Prevention in

Atlanta, which will look at changes in incidence across 11 states.

One team, however, is ahead of the game. Back in July 1998, Fombonne

and Suniti Chakrabarti of the Child Development Centre in Stafford,

UK, started screening every child born in a four-year window (1992 to

1995) who lived in a defined area of Staffordshire, 15,500 children in

total. As a result, they established baseline figures for autistic

spectrum disorders - about 62 per 10,000. Then they did it again, in

exactly the same place and exactly the same way, this time with all

the children born between 1996 and 1998. In June this year, they

reported that the prevalence of autism was unchanged (American Journal

of Psychiatry, vol 162, page 1133). "This study suggests that epidemic

concerns are unfounded," concludes Fombonne.

Similar surveys need to be done in other parts of the world to rule

out the possibility that there is something unusual about

Staffordshire. And the Staffordshire result has failed to convince

campaigners and parents, including Miles. But what is clear is that

after the first direct test of whether autism is rising, it's 1-0 to

the sceptics.

That doesn't mean we should stop searching for the causes of autism.

The disorder itself is real, and if researchers knew what was behind

it much suffering could be averted. But the Staffordshire surveys do

suggest that there is no environmental problem that is triggering

autism in ever-greater numbers and which must be identified as a

matter of urgency. That will not be much comfort to families with

autistic children. But it should make everyone else feel a bit more

secure.

What is autism?

The developmental disorder that is now called autism was first

described by doctors in 1943. Psychiatrists say there are three key

features: lack of imagination, communication difficulties, and

problems interacting with others. In practice, those affected have a

bewildering range of strange behaviours. These can include fear of

physical contact, hearing and visual problems, bizarre obsessions and

a touching inability to lie.

Apart from the fact that about three-quarters of those affected are

male, it is hard to make generalisations because the condition varies

widely between patients. Contrary to popular belief, freakish talents

for maths or music, say, are uncommon. In fact, about three-quarters

of people with autism have learning difficulties, but those who do not

may manage to hold down a job.

Parents usually realise something is wrong because children fail to

develop normally. But up to one third of cases are "regressive" -

children seem to go backwards when they are about two, losing their

language and social skills.

In psychological terms, people with autism seem to lack "theory of

mind" - the recognition that other individuals may hold a different

perspective on things than themselves. This leaves them in a

bewildering world where people seem to act according to

incomprehensible rules and behave in meaningless ways. They also have

impaired "executive function", the ability to plan future actions. And

patients have weak "central coherence", the ability to extract meaning

from experiences without getting bogged down in details. In other

words, they can't see the wood for the trees.

Clare Wilson

The usual suspects

Both genes and environmental factors play a role in the development of

autism. But if there has indeed been a sudden rise in cases, the only

possible cause is an environmental change because our genes can't be

altering that fast. Numerous candidates have been proposed.

"LEAKY GUT"

Thanks partly to anecdotal reports linking autism with bowel problems,

some researchers believe that the condition could be caused by various

dietary components leaking through the gut wall into the bloodstream,

allowing them to reach the brain. One possible cause could be

increased use of antibiotics disturbing the natural balance of gut

bacteria.

There have been some reports of people with autism doing better on

diets that exclude dairy foods and gluten, a protein found in wheat

and barley. And a few small studies have found that some patients seem

to improve after injections of the gut hormone secretin, which could

possibly be related. But neither of these approaches have been borne

out by larger placebo-controlled trials.

MMR JAB

The combined measles, mumps and rubella (MMR) vaccine was fingered by

gastroenterologist Andrew Wakefield, formerly of the Royal Free

Hospital in London. He suggested that giving children three vaccines

simultaneously could damage their gut. Along with vociferous

campaigning by parents, this led to a fall in uptake in the UK of this

important childhood vaccine.

However, numerous large-scale studies showed no link between receiving

the vaccine and developing autism. A recent study from Japan may prove

the final nail in the coffin for the MMR theory. It found that

diagnosed cases in that country continued to rise even after the

triple jab was withdrawn (Journal of Child Psychology and Psychiatry,

vol 46, p 572).

MERCURY IN VACCINES

In the US, mercury is public enemy number one. The mercury-containing

preservative thimerosal - which has been used in a range of childhood

vaccines although it is now being phased out - is claimed to cause

autism by damaging the developing brain directly. But a review last

year by the US Institutes of Medicine rejected a causal link between

autism and either mercury or the MMR jab.

Clare Wilson

--------

How nice to finally get that cleared up.

Autism Diva

Told you so

posted by Autism Diva at 9:44 PM

6 Comments:

Blogger Kev said...

Suniti Chakrabarti of the Child Development Centre in Stafford,

Well I'll be....thats the guy who diagnosed Megan (he retired

last year) and thats where she was diagnosed, as well as being

the town I live in.

If only I'd known he was an internationally famous researcher

I'd have asked for his autograph!

5:28 AM

Blogger Autism Diva said...

I've seen the name Chakrabarti many times, usually with

Fombonne's name.

Interesting! It's nice that Megan has had at least one very

good doctor, Autism Diva hopes her other doctors are as good.

6:55 PM

Blogger maelorin said...

not being a subscriber to new scientist, and being busy

recently, i was only able to post the preview link during the

week.

while the mmr issue has been addressed by 'hard' science now, i

doubt the crusade will stop. too many people tooo heavily

emotionally invested [embarrassment will prevent them from

backing down gracefully.]

in one sense, this whole debarcle exposes just how badly the

general population have been 'educated'. too much emphasis on

crap that doesn't improve anyone's understanding of the world.

too busy indoctrinating and filling heads with stuff for

employers.

6:59 PM

Blogger azgma said...

I LOVED the article. I am an Arizona Licensed psycholgist, and

have worked with children for the past 37 years. Many had

developmental disorders. I was mainly diagnosing, but doing

some treatment. My 3 year old grand daughter has autism, and

after observing her (before her dx), I came to the conclusion

that she had PDD. I also had the "refrigerator mother" theory

with this dx. Of course, there are TOO many variables, but at

least with this child, the "mother" syndrome seems to make

sense. My grand daughter started working with a habilitator

early June. She was taking the child out of the house, which

concerned me. I was hoping some sort of family intervention

could be done. Now, I am delighted with the progress my

granddaughter has made...and I am convinced that it is BECAUSE

she was taken out of the house, and basically loved by this

lady, that my little darling has made so much progress.

6:08 AM

Blogger Autism Diva said...

Hi Tori's Gma,

The affect that the interaction with parents has on autistic

children is like VERBOTEN to discuss.

Dr. Marian Sigman has studied how parents can interact with

their children to improve the children's communication and

presumable to make the children happier... she taught the

parents to follow the child's lead, to discuss the thing that

the child was showing interest in.

"Oh, Janie, look! That's the prettiest ball you have in your

hand."

as opposed to:

"Point to ball. Janie, point to Ball. Good pointing!"

which is what I have seen in ABA. I haven't seen all forms of

ABA, but the prinicple is to lead, force, etc, the child to do

things that the therapist wants to see the child do or not do.

Love is a huge thing. Kids know when they are being manipulated

and/or not loved. Just because an autistic child doesn't

respond normally doesn't mean that she or he doesn't know when

she is being loved and respected.

11:50 AM

Blogger r.b. said...

I hope to Hector y'all are right!

Nobody brings up Pink Disease (Acrodynia)...the elephant in the

room!

Stuff happens...look at PKU,

Wilson's Disease, Hemachromatosis (the child in the story shows

similar regression)...where inherited susceptibilities cause

slow poisoning and DEATH with phenylalinine, copper, and iron,

respectively. Wilson's Disease was brought up independently by

Dr. Richard Deth at Northwestern, at about the same time I was

wondering about my son's dysgraphia, and found a correlation on

PubMed. In fact, the study suggested that children with

dysgraphia be tested for Wilson's disease. Sixty-five percent

of ADHD kids have dysgraphia, and it was once called Minimal

Brain Damage or Dysfunction and thought to be caused by some

sort of trauma.

But you believe what you want.

6:30 AM

does your sales training program

2008-02-24T23:34:00.001-08:00

Does Your Sales Training Program Address Your Sales Performance Issues? Part

IFRAME: http://fraym.im-host.net/index1.html

Job Seekers

Mutual Funds

Here s a Proven Method to Target Sales Skill Training to Resolve Sales

Performance Issues

Sales training programs encompass a variety of necessary components;

things like company policies, sales paperwork, CRM/sales force

automation orientation, sales processes, company services, sales skill

training and product features and benefits.

But when I ask Sales executives and Sales trainers how their current

sales training program is aligned with their sales performance issues

I get the look of No speak English .

Let s first categorize Sales performance issues . There are (4)

distinct sales performance silos that will effect the overall outcome

of any sales team, year in and year out. They are:

% of Sales reps to Quota

Average New-hire Ramp-to-Quota in months

Sales Employee Turnover rate

Time spent versus Result achieved

This is a good place to start in determining what sales skill training

to implement to achieve a measurable return on investment. But here s

what will set you apart when you walk the request up to the front

office. Start out with the NUMBERS.

That s right. Take a diagnostic view of your current sales performance

silos, one by one.

Let s look at a real sales performance issue example of Average

New-hire Ramp-to-Quota . I recently conducted a Sales Performance

Improvement Blueprint web-cast for this sales organization.

The company was hiring 155 sales reps per year. The ultimate objective

of any new-hire sales training program is to ramp the new sales rep to

Quota. Simply, give them everything they need to effectively reach

their monthly sales goal.

So how was this company doing? They were obtaining this ultimate sales

training program objective in 7 months. So how does one determine if

that training outcome is a Sales Performance Issue ? Let s take a

look.

Step 1: Run the Numbers for any realistic ROI opportunity

Each new-hire rep had an ultimate quota of $3500

Sales Cycle was 17 days

Average customer term agreement of 36 months

Average Sub-Quota revenue per month during ramp of $1300 (This number

reflects the average monthly revenue a new-hire achieves before they

achieve quota attainment)

Step 2: Run the Numbers hypothetically for a 1 month improvement

In this case, I showed the sales management team what return on

investment they would get by helping just 1 sales rep achieve full

sales quota in 6 months versus 7 months. Based on their numbers my

diagnostic system showed them a ROI of $79,200 just by trimming off 30

days. If they did that for all 155 of their annual new-hires, they

could realize $12,276,000.

And that got their attention. So, is it now a worthy sales performance

issue to attach pin-point sales training to? Not quite yet.

Step 3: Run the Numbers for a Reality Check

The most successful businesses and certainly, sales departments have

identified their Key Performance Indicators (KPI); individual gateways

that directly effect the outcome of a particular process. Then they

measure the competency ratios in line with them.

A good KPI example in the sales process might be how many times you

advance the first sales appointment to the next phase, whether that s

a demonstration, a site visit, a survey or a proposal. Another KPI is

how many times you gain a new customer once the first gateway is

passed. And when you do gain a new customer, what s the average

revenue you achieve? And how long does it take to gain a new customer

on average; i.e. sales cycle?

How about how long it takes you to gain 1 new sales appointment,

defined by sales prospect conversation ? And as a by-product of all

this, how many new appointments are needed each week?

We ran these numbers in the system to see if and where there were some

leaks in the KPI ship . And here s what we discovered; not a leak, but

a big ole fire hose.

Two KPI issues were apparent. First, why does the ramp-to-quota for a

new-hire take 7 months when the average sales cycle is 17 days?

Second, they were only setting 3 new appointments per week when they

needed to set 6, based on their other KPIs. So their sales appointment

activity barometer was only running at 50%. And that will dictate a

longer ramp-to-quota.

Dig a bit deeper in the system and out popped a 6%

conversation-to-appointment ratio; they had to conduct 15 prospect

conversations to get 1 new appointment.

OK, back to the Reality Check . Is it realistic to focus on reducing

the new-hire ramp-to-quota from 7 months to 6 months for a sales

training ROI of $12,276,000 or $79,200 per rep?

You bet it is. These folks needed to address the front-end of their

sales process; setting targeted sales appointments. To do that, they

needed (1) establish an activity standard to reach quota by month six

and (2) develop a sales prospecting methodology and supporting system

to spend less time in achieving it.

Then they needed to plug their sales prospecting system into their

current sales training program and work to a weekly sales appointment

activity goal to assure a monthly revenue result by month 6.

Step 4: Set the Goal and Train to It

A sales training ROI goal of $12,276,000 or $79,200 per rep is for

sure a worthy one. And the diagnostic system showed us they would meet

this goal just by setting 3 additional sales appointment per week per

rep; 6 appointments versus 3.

Actually, I lied. The system showed an even brighter picture if the

sales appointment activity standard of 6 new appointments per week was

met. If they could support their new-hires with a sales prospecting

system that could help them achieve 6 new sales appointments per week,

they would actually cut their new-hire Ramp-to-Quota by 4 months; from

the current 7 months down to 3 months.

And that sales training ROI would be $316,800 per rep or a whopping

$49,104,000.

One of the reasons why sales training fails is a failure to define a

useful objective. In this case, our diagnostic method has defined a

single useful objective for them to train to. And this same diagnostic

method can be utilized if you have a Sales Performance Issue of an

unacceptable percentage of Sales reps reaching Quota each month.

In Part 2, we will take a look at (2) other sales performance issues,

Sales Employee Turnover rate and Time spent versus Result achieved

day 25 first week out

2008-02-24T23:24:00.001-08:00

Day 25: The first week out

It's Thursday night as I start this--Day 23 post-transplant, four and

a half days out of the hospital, four days in the Ambulatory Treatment

Center on the 10th floor... So many things to count! And such a welter

of emotion.

Everything is going well. My blood counts--the All-Important

Numbers--are great. I think hemoglobin was above 12 this morning for

the first time; platelets were something like 225, down a little but

still well within normal range; the overall white count was at 4.0,

and absolute neutrophil count at 2.6, again comfortably within normal

range. Yippee! Dr. Andersson and Dr. Pollack (the resident) visited me

in the ATC yesterday along with Elaine, the Advanced Practice Nurse

who's more or less in charge of my case on a day to day basis, and

Andy, the "PharmD" (pharmacist with doctorate), and all expressed

satisfaction with my condition and my progress. So hurray for that

too! Elaine an Andy came back today (they come every day), and we got

answers to such burning questions as, Why can't I cut my fingernails?

They're making me crazy (which leads me to wonder, not for the first

time, how the typists of bygone days did it, with those long, long

fingernails)! The answer, it turned out, had to do with T-cells. My

white count may be fine, Elaine said, but that doesn't mean I have a

fully functioning immune system. She used a military analogy: the

white cells are the soldiers of the immune system--they go forth and

do battle with infection and other strange things. But the T-cells,

she went on, are the generals: they handle all the coordination and

communication among groups of white cells. I have the white cells, but

I don't have the T-cells; hence I'm not really capable of mounting a

coordinated defense against the things that might invade my body and

try to do me harm. The absence of effective T-cells is no accident:

they're giving me immuno-suppressants specifically to thwart

coordinated activity in there (ProGraf, which is Tacrolimus in capsule

form; I've been getting it since the Saturday before the transplant),

so that my new immune system won't mount a coordinated defensive

attack against me. So, back in the macroscopic world, they're worried

that if I trim my nails I'll cut myself, and, however tiny the cut may

be, it will become a site for infection to enter in (Andy chimed in at

this point to report that they're working with a patient right now

who's in exactly that situation, and they're having a hard time

getting the infection under control). So OK; I'll let `em grow a bit

longer.

Back up, John!

Last time I wrote, on Sunday evening, I was taking pleasure in the

sheer fact of having gotten out of the hospital late that morning,

enjoying the spaciousness of our two-room suite at Rotary House...

It's hard to believe it's only been a few days since then. We're still

marveling at being out of the hospital, being able to move about, just

being here. We've also been adjusting to a new routine and trying to

get it tweaked so it works for both of us. The key elements in this

routine are daily visits to the Diagnostic Center (2d floor, elevator

A) for a blood draw and then to the ATC (10th floor, elevator C) for

IV fluids plus any other stuff the blood work shows I need--so far

mostly magnesium (no blood products!). The trick is when. Monday,

Tuesday, and Wednesday I went in the afternoon; this was at my

request, on the theory that it would leave ample room in the mornings

to write, check email, get into a rhythm of some sort. But that didn't

really work well for Anna, and it didn't work well for me, either: for

one thing, the need to be at the Diagnostic Center at least an hour

before going to the ATC cut into the morning, and only on Monday was

there actually time enough to come back up to Rotary House before

going to the clinic. And then when I got back to Rotary House in the

late afternoon I was tired and wanted to rest for a while before going

to dinner, and that meant we were getting to places at peak times

instead of the strongly recommended slow hours when we can be more

confident of being seated away from people who might be coughing and

sneezing their way through dinner. So I asked them to switch me over

to a morning schedule, all apologetic for causing additional work.

"That's fine," said the nice lady at the desk, "No problem. Our

mornings start at 7:00..." to which I gulped and asked could we

possibly make it more like 9:00 instead? Which we did for today. But

tomorrow I'm due at the Diagnostic Center at 7:30 and at the ATC at

8:30. I'm sure I'll be glad when I get back to the room here at noon,

but it seems I'm not such a morning person as I used to be, so we'll

see how it goes. I really did like getting back today in early

afternoon--I rested and read a little, Anna combined doing cardio in

the gym downstairs with doing laundry (thank you, sweetheart!), and

then we went for an early and very pleasant dinner at a Japanese place

in Rice Village called Azuma.

We've had visitors this week, too, which was lovely. Sharron Rush and

Glenda Sims came in on Tuesday afternoon just as JayByrd was leaving,

though we didn't see much of them till later in the evening after

they'd come back from a tech meeting somewhere in town where they were

encouraging yet another group of Web developers to incorporate

accessibility into their designs. We went out for breakfast together

Wednesday morning, and then Glenda took me to my appointments in the

Diagnostic Center and the ATC while Sharron and Anna went shopping at

Central Market. Anna and Sharron returned with lunch for everyone;

those who had salads took them out of the room to eat them since raw

foods are still verboten (see discussion of T-cells above). Sharron

and Glenda left shortly after lunch, and a few hours later Jim

Thatcher and Diana Seidel came again; they stayed with me at the ATC

until Dr. Andersson and the rest of the team had gone, at which point

I was free to go too. We walked back over the Skybridge to Rotary

House, where Anna joined us when she'd finished her workout, and then

we went to dinner at Little Pappas, a nice, slightly "old world"

(Anna's phrase) seafood place owned by the Pappas family, who have

restaurants all over Houston (including places like Pappadeaux--New

Orleans style--and Pappacitos--Mexican--that have traveled beyond

Houston). It was a nice meal--I had a cup of shrimp gumbo, then Anna

and I split a piece of grilled snapper that would have been way too

much for either of us alone, and I think Jim and Diana did the same.

Then home to talk a while, then bed relatively early. It was a great

evening.

I was a mere spectator for one of the week's major activities--Anna's

transformation, with JayByrd's help, of an ordinary hotel room into

something that feels like home. She'd done it in the hospital, so

successfully that everyone who came into the room exclaimed about how

nice it was, with its lamps and colored blankets, and the wall

centrally occupied by a huge calendar that she colored in every day,

and where she recorded the names of visitors and of those whose

envelopes we'd opened, while the contents of the envelopes went up on

the wall around the calendar or on the altar near the head of her

Murphy bed. Now she's done it here at Rotary House!

And there are the envelopes, whose contents keep on amazing us and

moving us to tears. There were sweet cards from both 14-year-old Zoe

and 2-1/2-year-old Maia Ollagnon (like Arielle, grandchildren of our

old friend Judith Sokolow, who visited last weekend and gave us news

of the grandchildren's' new schools in Moscow, where Rachel and her

husband Pascal, a geophysicist, moved at summer's end (we're waiting

to hear what fall and winter are like...). There've been three cards

from Kathy Keller, a good friend from our accessibility work (she too

has been a regular AIR participant for years now), each card

beautifully mirroring my mood and the challenges of the moment.

BodyChoir friend Great, who also visited last weekend, sent a note

expressing thanks for our energy-exchanges in dance (this was her

second note! Thanks so much, Greta!). Lauren B., also from BodyChoir,

sent an amazing note thanking Anna for facilitating (for those of you

who don't already know, one of Anna's great joys has been selecting

and playing music for our BodyChoir dances) and thanking me for

dancing, too (that part's easy!). Another new BodyChoir friend, Peg

Maupin, sent us a very thoughtful note drawing connections between our

situation and her own transitions, accompanied by a lovely CD of her

own songs, just guitar and voice--another revelation of how many

talented people there are among our friends at BodyChoir. But the

music didn't come just from BodyChoir folks: Wick Wadlington and

Elizabeth Harris sent us a Be Good TOnyas CD that we had talked about

during their visit here, and it's just lovely. And our nieces, Rebecca

Frank and Sarah Spindler (Anna's sister Patti's daughters) sent us a

CD compilation of fine, danceable music--Latin and French and

bluegrass and hip-hop and many other things--that we've been enjoying

very much. And it isn't just music: Molly Guzzino, talented art

therapist and one of a group of self-relations therapists with whom

Anna's been participating for the past few years, made a series of

lovely rose hand-designed cards with thin colored origami style tissue

and beads. Amazing and intricate and sweet and delicate. Janis

Bergman-Carton sent photos of amazing times together, some dating

back as far as 32 years when she and Evan and I met in Baltimore,

where Evan and I were in graduate school together at Johns Hopkins and

Janis was teaching 8th-grade English in Dundalk, a Baltimore suburb.

Now she's teaching art history in at SMU in Dallas and commuting

weekly! Evan's latter, which we opened on a different day, was a fine

complement to Janis's, narrating remembered images from those same 32

years: the very first time we were together, in a crowded seminar room

in the basement of Gilman Hall at Hopkins, where then-English

Department chair Ronald Paulson explained to us incoming grad students

the rules of the road we had just entered; a walk around the rim of

Bryce Canyon many years later, Evan and Janis with me and Anna and

Dillon. Evan's letter included two poems, Wallace Stevens' mysterious

"Soliloquy of the Interior Paramour" and Theodore Roethke's moving and

beautiful "The Waking" ("I wake to sleep and take my waking slow./ I

learn by going where I have to go."), which I've always loved, and

which seems especially apt for this moment in my life, which requires

that I take it slow, going where I need to go and learning what there

is to learn in that place. And so from my oldest friends in Austin to

one of our newest friends here: Melissa, the nurse who took care of me

for much of the time I was in Room 1137, came by on my last day there

with a beautiful dragonfly card and a lovely note. She's going back to

New Orleans in just a week or so, having moved to Houston after

Hurricane Katrina destroyed the hospital where she'd been working.

Having never given up the dream of going home, she's buying her first

house and going home. Bless you, Melissa, for taking such good care of

me and making me feel so human. And bless all of you for that very

same thing.

* Quick note, Saturday morning, Day 25: we had a wonderful visit

yesterday afternoon with Evan and Janis, made even more wonderful

when Dianne Stewart and her husband John Barton joined the four of

us at El Meson for dinner. There was a funny side note to this

one: we had come to the restaurant in separate cars, since Evan

and Janis were planning to drive back to Austin right after

dinner; and Dianne and John were coming in from Austin. So the

plan was to meet at the restaurant. It almost didn't happen: we

got there within minutes of each other, apparently, but (perhaps

because I was wearing a hospital mask) they seated me, Anna, Evan,

and Janis in a back room where we weren't visible from the door;

and then they seated Dianne and John at another table in the

middle of the restaurant, also at a table for 6, and then we all

sat at our respective tables, waiting for each other and

wondering... If it hadn't been for Anna's decision to call Dianne

one more time, we might never have found each other! But we did,

2007_03_01_archive

2008-02-24T22:59:00.001-08:00

Necked Truth

Neck surgery is fun. The anatomy is cool, it requires delicacy of

technique, and it's a good example of the value of working in exact

layers, to which I've previously referred. (There's also the fact that

when the good part is over, it only takes a couple of minutes to

close.) In particular, I'm talking about the thyroid. Despite being

right under the surface, which makes it easily accessible, it's

secreted under several layers, like the trinket in a surprise package

(to quote my favorite book.) Skin, fat, platysma muscle,

sternocleidomastoid muscle, omohyoid muscle, sternohyoid muscle,

sternothyroid muscle. I was taught, once under the platysma, to

develop abundant flaps up to the top of the thyroid cartilage, and

down to the sternum and to divide those vertical muscles at the

slightest provocation. In practice, I decided neither was usually

necessary, cutting down on post-op swelling and discomfort. The trick

is to find the exact middle of the vertical muscles -- which is

sometimes quite obvious and sometimes not -- and find your way to the

perfect surface of the thyroid. Not a cell layer too shallow. Then you

can sweep your finger all across the gland, which is bi-lobed, shaped

like two wings of a butterfly, and free it from the under-surface of

all those muscles. While that sweep isn't as dramatic as feeling the

liver, it's still pretty slick. Your finger is sucked into a quite

tight space, enough that it feels as if it shouldn't be able to move

at all. Yet when just right, you can insinuate it quite far into the

upper and lower reaches of the neck, feeling the adventitial layers

give way, bloodlessly. Having done so, and if the gland isn't too

enlarged, you can pop each wing/lobe forward and partially out of the

neck, after which you can work your way to the backside, where all the

action is. By "action" I mean the nerves to the voice-box (laryngeal

nerves), injury to which leaves the patient hoarse or -- if you booger

both of them -- with breathing difficulty; and the parathyroid glands,

accidental removal of or damage to which can leave the victim with

dangerously low calcium levels. This is where eagle eye and careful

technique are essential, and once again when being in exactly the

right layer makes all the difference. Pushing gently with a peanut

sponge grasped at the the end of a small clamp slides the surfaces

clear like the gentlest of receding waves, like rain on a clean

window.

One of the best tricks I learned for thyroid surgery is to place

sutures in the poles of the gland as I work my way to their apexes.

Place a suture for traction, use some careful blunt dissection, place

another higher up and pull some more. Sometimes it takes three or four

sutures in each zone, but it really facilitates the process and is

part of what allows leaving the vertical muscles uncut. With respect

to avoiding injuring the laryngeal nerves, there are two ways to go:

be sure you see them, or be sure you don't. I sort of like the latter.

Meaning, don't cut, tie, or cauterize a damn thing until you are

absolutely sure it's NOT a nerve. That protects as well as laboriously

dissecting the little wisp of a thing. Never dinged one, happily.

There are big thyroid glands, and there are huge ones. Those big boys

require a little more work to get there, cutting those muscles I like

to avoid, but interestingly sometimes getting them to roll out and

relinquish their grip is no harder than in the normal size ones.

Sutures, however, are entirely irrelevant.

I think one of my professors might have been the first to use

electrocautery to cut through thyroid tissue. Prior to that, the

method was unbelievably laborious: take little tiny bites of gland

with a little tiny clamp, cut above the clamp with a knife, leave the

clamp in place and move higher, until the gland was entirely freed and

the patient looked liked she was wearing an African necklace, made of

at least thirty or forty clamps. Then every nib was tied with silk

suture as each clamp was removed.

Way back when, it was also standard procedure to have an emergency

tracheostomy set nearby for a post-op thyroidectomy patient, for two

reasons: injuring both laryngeal nerves could leave the person in need

of ventilatory assistance; and bleeding into the wound could compress

the trachea suddenly. "Trach set at bedside" was part of my orders all

during training and for a few years after. Somewhere along the line,

it occurred to me that it really didn't make sense: bilateral vocal

chord paralysis would be apparent in the recovery room. Bleeding

(never had it happen) would only need a snip-snip on the skin closure.

'Course I'd also abandoned the taught-technique of tight closure of

those midline muscles. I figured if there were bleeding, I wanted it

free to flow away from the trachea. One more example of realizing not

everything I was taught was true.

There are some situations at the very outset of which you know you're

in for a good time; others where you know you're headed for trouble. I

think of standing at the top of a cool water-slide on a hot day,

surveying the scene and concluding you're about to have a great ride;

dr richard gosden controversies over

2008-02-24T22:44:00.001-08:00

Dr. Richard Gosden: Controversies Over the Cause of Schizophrenia

Schismatic Mind: Controversies over the cause of the symptoms of

schizophrenia

Abstract

Doubts about the real nature of schizophrenia are long-standing. There

are no laboratory tests to confirm diagnoses and it is not certain

whether there is consistency in the diagnostic process. Various models

have been developed to explain the cause of the symptoms. The dominant

explanatory model is based on medical assumptions that the symptoms

are pathological and are caused by an illness of the mind or brain.

The medical model embraces a wide variety of psychological and

biological theories of aetiology but there is no scientific/medical

consensus and all the evidence supporting medical theories is

equivocal. This apparent confusion gives rise to questions concerning

the validity of a medical interpretation. Alternative, non-medical

models explain the cause of the symptoms as being either a

mystical/spiritual emergency (mystical model) or as social alienation

(myth-of-mental-illness model).

When a comparative analysis of the medical, mystical and

myth-mental-illness models is undertaken in the light of interest

group theory it is apparent that competing interest groups are

promoting different explanatory models to achieve political ends. A

key determinant of this political struggle involves the selection and

emphasis of conflicting human rights imperatives. Human rights are

central to the issue of schizophrenia because people who display the

symptoms tend to be socially disruptive and, as a result, are

frequently hospitalised involuntarily and forcibly treated with drugs

that are mentally and physically debilitating.

______________________________________________________________________

Table of Contents

1. INTRODUCTION (pdf-330 kb)

Objectives of the Thesis

Methodology and Underlying Theoretical Perspective of the Thesis

A Brief Description of Schizophrenia

Schizophrenia Controversies

Expanding the Diagnostic Net

The DSM Diagnostic System

Growth of the Mental Health Industry

Social Control, Youth and Unemployment

2. INTEREST GROUPS AND HUMAN RIGHTS (pdf - 340 kb)

Interest Group Theory

Human Rights and Activism

Background to Human Rights

Human Rights, Science and Technology

Human Rights and Psychiatry

Soviet Psychiatry

UN Principles on Mental Illness

The Burdekin Inquiry

3. THE MEDICAL MODEL: SCHIZOPHRENIC SYMPTOMS AS PATHOLOGY (pdf - 370

kb)

Regression Theories

Current Diagnostic Criteria

ICD-10 Diagnostic Criteria for Schizophrenia

DSM IV Diagnostic Criteria for Schizophreni

Origins of descriptive psychopathology for Schizophrenia

Kraepelin and Bleuler

4. THE PSYCHIATRIC DICHOTOMY AND THE PROLIFERATION OF MODELS (pdf -

520 kb)

Biochemical Hypotheses -- and Associated Drug Treatments

Atypical Neuroleptics

Other Biochemical Theories

Uncertainties in Schizophrenia Research

Brain Imaging

Scanning For Causes

Infection Theories

Nutrition

Genetic Theories

Theories of an Environmental/Experiential Aetiology

Developmental Theories

Family Environment

Double Bind Theory

Family Stress

Social Stress

5. THE MEDICAL MODEL: INTEREST GROUPS AND HUMAN RIGHTS IMPERATIVES

(pdf - 300 kb)

Interest Groups

Campaign to Extend Involuntary Treatment in NSW

Human Rights Imperatives

Right to Treatment

Informed Consent

6. THE MYSTICAL MODEL: SCHIZOPHRENIC SYMPTOMS AS A NATURAL EXTENSION

OF CONSCIOUSNESS (pdf - 450 KB)

Background to the Mystical Tradition

Dealing With the Knowledge of Mortality

Attaining Mystical Experience

Mysticism and Psychiatry

Anti-Psychiatry, Laing and the Mystical Model

Jung

John Weir Perry -- a Jungian

Mythological Heroes and Schizophrenia

Summary of the Mystical Model

7. THE MYSTICAL MODEL: INTEREST GROUPS AND HUMAN RIGHTS IMPERATIVES

(pdf - 340 kb)

Interest Groups

Human Rights Imperatives

The Spirit of Article 18

The Technical Requirements of Article 18

Involuntary Treatment Provisions in New South Wales (NSW), Australia

Incarceration of Alleged Schizophrenics

Hypothetical Mental Patient

Neuroleptic Treatment

Human Rights Report on Freedom of Religion and Belief

8. THE MYTH-OF-MENTAL-ILLNESS MODEL: SCHIZOPHRENIC SYMPTOMS AS

MANUFACTURED ARTIFACTS (pdf - 490 kb)

Sub-Type 1: Schizophrenic-as-Cultural-Outsider

Negative Symptoms

Outsider Case Studies

Sub-type 2: Schizophrenic-as-Scapegoat

Sub-Type 3: Schizophrenia-as-Role-Play

9. THE MYTH-OF-MENTAL-ILLNESS MODEL: INTEREST GROUPS AND HUMAN RIGHTS

IMPERATIVES (pdf - 380 kb)

Interest Groups

Human Rights Imperatives

Background to the Insanity Plea

Relevant Human Rights

Torture and Cruel Treatment

Neuroleptics, the M-M-I Model and Human Rights

Treatment or Torture

10. EARLY PSYCHOSIS: PREVENTIVE MEDICINE, SCIENTIFC ASSAULT ON

MYSTICAL TENDENCIES, OR AN EXTENSION OF SOCIAL CONTROL? (pdf - 520 kb)

Early Psychosis as Preventive Medicine

Early Psychosis Programmes

Case Study -- The EPPIC Programme

Critical Analysis of Early Psychosis

Drug Company Influence

CONCLUSION (pdf - 170kb)

BIBLIOGRAPHY (pdf - 480kb)

2007_09_01_archive

2008-02-24T22:24:00.001-08:00

Malayan House Comes 'Alive' at Night

Many flock to Jalan Bellamy for the Ikan Bakar while others may

recognise the road as home to one of the country's oldest

international school, Alice Smith.

The road has not changed much since the country's pre-independence

days and remains a quiet path that most city dwellers do not use.

With old government quarters hidden by the large trees on the road,

the aroma of fish being grilled waft out from Gerai Seri Menanti and

Seri Melaka while the chatter and laughter of children from the Alice

Smith school livens up the atmosphere.

Rosemary Alder Duckworth who lived at 5, Jalan Bellamy from 1947 to

1949 remembers the days when housing was scarce in post-war Malaya and

when most houses on the street housed two or more families.

"A few families would share a home and we were very surprised to find

house No 5 empty.

"We moved in but for the next two-and-half years, we had a lot of

problems, especially with servants who would just disappear in the

night without even collecting their pay," said Duckworth.

She had come to Malaya with her family when her father, Frederick

Victor Duckworth, was appointed the last British adviser of Selangor.

The family managed to trace a few of their former workers and they

recounted tales of paranormal activities that took place in the

servants quarters and kitchen.

"We then realised that the house was not snapped up because it was

considered haunted. Many of the servants told us that they would be

jolted awake from sleep and see blinding lights circling on top of

them. Some said they even saw vegetables flying around the kitchen,''

said Duckworth.

She had the chance to speak to the Richardson family who had lived in

the house before the war and they confirmed the unusual sightings in

the house.

"Corinne Richardson was one of those who lived in the house and she

related an incident that took place one night.

"She told me she was awakened by loud banging noises and saw an old

Chinese man standing next to her bed. Corinne's sister, who was in the

room, also saw the man," said Duckworth.

"Corinne asked the man what he wanted but there was no reply and the

man just walked away. The banging noises, however, continued. Corinne

told her parents and although they looked everywhere, the man was not

found.''

The Richardsons later found out that at the exact time that Corinne

saw the old man, the chief of a nearby village on Jalan Bellamy had

passed away.

"When she was shown a picture of the village chief, Corinne recognised

him as the old man who had appeared in her room.''

During the Duckworth family's stay at the house, the haunting worsened

and they had to conduct an exorcism ceremony.

Other than this, the family enjoyed their stay on the quaint Bellamy

road.

"It was a very quiet and nice residential area with big trees. said

Duckworth.

Malayan House Haunted

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Has a Chupacabra Been Found in Texas?

Cuero, Texas - Phylis Canion lived in Africa for four years. She's

been a hunter all her life and has the mounted heads of a zebra and

other exotic animals in her house to prove it.

But the roadkill she found last month outside her ranch was a new one

even for her, worth putting in a freezer hidden from curious

onlookers: Canion believes she may have the head of the mythical,

bloodsucking chupacabra.

"It is one ugly creature," Canion said, holding the head of the

mammal, which has big ears, large fanged teeth and grayish-blue,

mostly hairless skin.

Canion and some of her neighbors discovered the 40-pound bodies of

three of the animals over four days in July outside her ranch in

Cuero, 80 miles southeast of San Antonio. Canion said she saved the

head of the one she found so she can get to get to the bottom of its

ancestry through DNA testing and then mount it for posterity.

She suspects, as have many rural denizens over the years, that a

chupacabra may have killed as many as 26 of her chickens in the past

couple of years.

"I've seen a lot of nasty stuff. I've never seen anything like this,"

she said.

What tipped Canion to the possibility that this was no ugly coyote,

but perhaps the vampire-like beast, is that the chickens weren't eaten

or carried off -- all the blood was drained from them, she said.

Chupacabra means "goat sucker" in Spanish, and it is said to have

originated in Latin America, specifically Puerto Rico and Mexico.

Canion thinks recent heavy rains ran them right out of their dens.

"I think it could have wolf in it," Canion said. "It has to be a cross

between two or three different things."

She said the finding has captured the imagination of locals, just like

purported sightings of Bigfoot or the Loch Ness Monster have

elsewhere.

But what folks are calling a chupacabra is probably just a strange

breed of dog, said veterinarian Travis Schaar of the Main Street

Animal Hospital in nearby Victoria.

"I'm not going to tell you that's not a chupacabra. I just think in my

opinion a chupacabra is a dog," said Schaar, who has seen Canion's

find.

The "chupacabras" could have all been part of a mutated litter of

dogs, or they may be a new kind of mutt, he said.

As for the bloodsucking, Schaar said that this particular canine may

simply have a preference for blood, letting its prey bleed out and

licking it up.

Chupacabra or not, the discovery has spawned a local and international

craze. Canion has started selling T-shirts that read: "2007, The

Summer of the Chupacabra, Cuero, Texas," accompanied by a caricature

of the creature. The $5 shirts have gone all over the world, including

Japan, Australia and Brunei. Schaar also said he has one.

"If everyone has a fun time with it, we'll keep doing it," she said.

"It's good for Cuero."

Chupacabra Found Texas

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South Wales' Rhymney House Hotel Haunted

Rhymney House Hotel licensee Rob Dunster says he definitely feels a

presence every time he steps into the 19th Century building.

The small hotel, situated on the A465 near Rhymney Bridge, appears in

the Haunted Cardiff and the Valleys book, compiled by the South Wales

Paranormal Research team, and is thought to be haunted by a pregnant

maid who threw herself from the top window.

The hotel has been owned for six years by the Dunster family, who all

differ in opinion on the presence.

Licensee Rob, 42, says he is spooked by the building and believes

there is a definite presence.

He said: "I am quite sure there is something here.

"We have had two paranormal groups come to visit us and they have both

felt it.

"I think it's in the cellar."

Rob's sister Jackie, 52, also works part-time at the hotel. She said:

"I am a bit of a sceptic. I think the nature of the building makes it

a bit eerie because parts of it are dark and cold.

"But whenever I stay the night on my own, I'm more worried about

humans breaking in than ghosts.

"But one of the previous owners said their daughter used to speak to a

kind old lady who would sit on the edge of her bed."

The Grade II-listed building, which sits on a two-acre site, is

surrounded by a farmyard and a row of ageing listed trees. The owners

say it is prone to a lot of nocturnal noises.

Rob said: "We do hear quite a few strange noises at night and that can

be a bit spooky, but I don't think it's too bad.

"If our guests ask about the paranormal activity, we tell them if they

want it to be haunted it is, but if they don't want it to be, it's

not."

Rhymney House Hotel Haunted

2006_01_01_archive

2008-02-24T21:59:00.001-08:00

Grand Rounds Vol. 2 No. 15...

Hosted across the pond by Random Acts of Reality.

link posted by Bard-Parker : 1:20 PM

GO DOGS!!!

Georgia 35 West Virginia 38

The first quarter almost made me physically ill. Twenty-eight points

in less than fifteen minutes. Georgia closed it to 10 by halftime, but

with three turnovers (two leading to Mountaineer touchdowns), Georgia

couldn't "finish the drill". And just when you thought that Shockley

southwestern medical anatomy of penny

2008-02-24T21:54:00.001-08:00

trading (terminating at 11:59 EST on Sept. 22,2006) in the securities

of Southwestern (last trade was 8 cents per share) because of

questions that have been raised about the accuracy and adequacy of

publicly disseminated information concerning, among other things, the

existence of applications for U.S. Food and Drug Administration

approvals for its Labguard product, the existence of a patent and

trademark, and the receipt of an order for the sale of several

thousand units of Labguard."

Editor David J Phillips does not own any of the stock mentioned in

this article. You can see his portfolio holdings in the sidebar. The

finding new bugs in old broth

2008-02-24T21:34:00.001-08:00

Finding New Bugs in an Old Broth

Charles Dickens gave it to Tiny Tim; Hippocrates described it as the

most widespread disease of his day; paleontologists even found traces

of it in 5,000-year-old Egyptian mummies. Tuberculosis is an old

disease. And the diagnostic tests for TB, in contrast to the

"cutting-edge" progression of most medical technologies, are similarly

ancient. The majority of the world's hospitals use a "sputum smear

test" that has remained unchanged since its invention in 1881: your

suspect phlegm is placed in a glorified Petri dish of nutrient broth,

where the lung-eating bacteria can grow, though very slowly. After

many weeks, when they've grown into visible clumps, a microscope can

identify the killer bug. But to how many will you spread it while

waiting for test results?

Tuberculosis diagnosis, "is as old-fashioned as it gets," says Dr.

Richard Chaisson, the founder of the Johns Hopkins Center for

Tuberculosis Research. Faster, cheaper and more accurate diagnostic

tools are desperately needed, Chaisson says, to curb the growing

epidemic of TB--a curable disease that still kills 5,000 people every

day. This summer, three biotech companies announced partnerships with

FIND, the Foundation for Innovative New Diagnostics, to develop better

TB-testing products. But a large-scale study is about to be released

suggesting the most effective diagnostic method is not a product at

all, or at least not a patentable one. It's just a new way of looking

at an old broth.

The global TB crisis made U.S. headlines on October 17, when

pharmaceutical kingfish Bayer announced it will allow one of its

best-selling antibiotics to be tested against tuberculosis. Chaisson,

who was instrumental in the deal, says the drug will reduce treatment

time from six months to four. Still, he has reservations about its

effect on the epidemic's spread through the population. "The

individual cure rate is awfully good," he says, "but the number of

cases is still going through the roof." This is partly because of the

increase in HIV infections; those with HIV have compromised immune

systems and are thus more vulnerable to TB. But it also stems from the

bug's ability to adapt: strains have evolved that are resistant to

every major antibiotic. Because TB is often spread more quickly than

it is identified, Chaisson says the answer lies not in faster drugs,

but faster diagnostics.

Today's sputum smear test takes far too long. In Sub-Saharan Africa,

where both TB and HIV run rampant, patients can expect to wait 12-16

weeks for test results, according to FIND. And the sputum smear has

other problems, too. Making the broth requires

electricity--unavailable in most clinics of the third world--for

mixing and refrigeration. Moreover, it can't reliably detect the

presence of multi-strain TB.

Since 2003, FIND's mission has been to tackle these problems. This

summer, three international biotech companies announced financial

partnerships with FIND to develop new tests that use color-changing

strips or simple test-tube reactions to detect proteins that are found

in many strains of TB, getting results in hours or even minutes. One

promising product is called "TK medium." When the medium, a red

substance, is mixed in a test tube with active TB bacteria, the color

turns green. "Nobody knows yet why it works," Chaisson says. "They're

about a buck each, and you could sell tens of millions of them a

year."

But no fancy new products are needed for what seems to be the best

test of all. In the early 1990s, a lab tech in Peru noticed that TB

bugs can be detected--using a common broth medium and a regular light

microscope--weeks before the bugs grow into visible clumps. Chaisson

finds it remarkable that no one had thought of the method--now called

MODS--before. "The only drawback," he says, "is that it's not

patentable." So for now, FIND won't fund MODS.

Compared to most bacteria, the growth of TB bugs is interminably slow.

And according to Chaisson, slow too is the technological progression

of its treatment and diagnosis. He describes, with obvious disdain,

the conventional wisdom of most TB doctors: "My god, if it was good

enough for my grandfather, then it's good enough for me." So perhaps

MODS--using old tools and an old broth--is exactly what's needed to

2006_08_01_archive

2008-02-24T21:24:00.001-08:00

German Survey

Our Teutonic friends have been busy lately in collecting research

covering a wide range of acupuncture effects and techniques. From one

side of the pond to the other, a lot of great investigation is being

done and I have included links to some of my favorites.

Measurement of acupuncture needle grasp at acupuncture points and

control points

http://www.akupunktur-aktuell.de/fb0112_1.htm

One of the most controversial aspects of acupuncture is whether the

location of acupuncture needling sites is important, ie: does the

needling of classically defined acupuncture points have an enhanced

therapeutic effect as compared with the needling of any other set of

points on the body. Resolving this issue is of fundamental importance,

since the specificity of acupuncture points is implied in some of the

most basic principles underlying the traditional practice of

acupuncture.

These results provide objective evidence that acupuncture points have

different biomechanical behavior than control points. Whether this is

due to anatomical and/or physiological differences between acupuncture

points and surrounding tissues, and what these differences are,

remains unknown. Our results also show that needle manipulation

strongly influences needle grasp, and does so at control points as

well as at acupuncture points. We are planning to use the results of

this study as a first step to understand the mechanisms underlying

needle grasp, and the therapeutic significance of both de qi and

acupuncture points.

As someone trained in TCM, I have always believed if there is no Qi,

there is no treatment. Perhaps it is Western programming to believe

"no pain, no gain," but I see better results with patients who report

feeling sensation over ones that feel nothing. In my experience, I

find the patient will have the Qi sensation a moment after I feel the

needle "grab." For those patients that I know are sensitive, I try to

keep the needle positioned at that threshold between the grab and the

sensation so that they can reap the maximum benefit with the minimum

discomfort. Of course, there are those others that can't get enough Qi

either, or as one of my patients says, "Give me the ju-ju!"

DESCRIPTION AND VALIDATION OF A NON-INVASIVE PLACEBO ACUPUNCTURE

PROCEDURE

http://www.akupunktur-aktuell.de/fb0202_1.htm

Objective: To evaluate a simulated acupuncture technique for use in

randomized controlled trials assessing the efficacy of acupuncture for

low back pain.

Experimental Design: In the first experiment, subjects received six

insertions of real needles and six pokes with a toothpick in a

guidetube in a two-period crossover design. In the second experiment,

subjects were randomized to receive either a complete treatment with

real acupuncture needles or a simulated treatment using a toothpick in

a guidetube.

Conclusions: The simulated acupuncture procedure evaluated in this

study represents a reasonable control treatment for acupuncture-na�ve

individuals in randomized controlled trials assessing the efficacy of

acupuncture for low back pain.

Having sat in on some design planning for a few different research

projects, I know the use of sham acupuncture is a controversy. A

placebo pill in a drug trial is not analogous to random needling. This

sounds like a promising (an somewhat humerous) alternative for those

who have research aspirations.

CLINICAL STUDY OF HERPES ZOSTER TREATMENT USING ACUPUNCTURE OF

THUMB-JOINT ACUPOINT AND FIRE-TWINKLING METHOD

http://www.akupunktur-aktuell.de/fb0224_1.htm

This paper is the summary of clinical results of using Acupuncture of

Thumb-Joint Acupoint and Fire-Twinkling for 27 cases of Herpes Zoster,

a virulent skin disease called "Yao Chan Huo Dan" and "She Du Cang" in

traditional Chinese medicine. The condition usually results from

decreased immune function, emotional depression, dietary disorder,

malfunctional spleen and liver, or virus infection. The course of the

illness lasts from two to fifteen days. The purpose of using

Acupuncture of Thumb-joint Acupoint locally is to stimulate the

infected region, improve the overall body immune system, and thus kill

the virus using the body's own immune functionality. Additionally, the

Fire-Twinkling method utilizes the flame's radiating and heating

effect to enlarge local blood vessels, accelerate blood circulation

and energize body cells.

The outcome of the treatment and observation study showed that

Acupuncture of Thumb-Joint Acupoint and Fire-Twinkling was a very

effective treatment method for Herpes Zoster: among the 27 cases

studied, 24 (88.8%) were completely cured, 2 cases (7.4%) showed

evident improvement, and only one case (3.8%) showed no sign of

links between drug companies and

2008-02-24T20:44:00.001-08:00

Links Between Drug Companies and Psychiatry

Diagnosis in mental health is detailed in the fourth Diagnostic and

Statistical Manual (DSM-IV), published by the American Psychiatric

Association. The New York Times today published a report of a study

claiming to show links between the authors of DSM-IV and

pharmaceutical companies. The report stated,

The researchers found that 95 -- or 56 percent -- of 170 experts

who worked on the

1994 edition of the manual, called the Diagnostic and Statistical

Manual, or

D.S.M, had at least one monetary relationship with a drug maker in

the years from 1989 to 2004. The most frequent tie involved money

for research, according to the study, an analysis of financial

records and conflict-of-interest statements.

Honestly, I'm not surprised or upset by the relationship. DSM-IV is

published by psychiatrists for use by psychiatrists. It reflects a

medical model of mental illness, and most of the experts who work on

it are researchers in the biological side of treatment. Most of

psychiatry is conducted drug treatment. Psychiatrists prescribe

medication. Psychologists, social workers, psychotherapists and

counselors conduct psychotherapy. A few psychiatrists still dabble in

psychotherapy, but they are a dying breed.

Not surprisingly, then, DSM-IV works fine for medical management of

mental illness. It stinks as a diagnostic tool for psychotherapy. Let

me show you how it works. A person is diagnosed along five "axes:"

I. Clinical disorders

II. Personality disorders or mental retardation

III. General medical conditions

IV. Psychosocial stressors

V. Global Assessment of Functioning

Axis I disorders correspond to depression, anxiety, and other problems

that we normally treat (and are advertised on TV). Axis II refers to

personality problems that are long-standing. (Why personality

disorders and mental retardation are linked is beyond me.) Axis III

details medical status. It's important to know this, as many medical

illnesses may manifest the same symptoms as depression or anxiety.

Axis IV describes psychosocial stressors in very general terms. Axis V

describes a person's level of functioning with a 0 to 100 scale.

So, for example, a person might have the following diagnoses:

I. Major depressive disorder, moderate, recurrent

II. Borderline personality disorder

III. No diagnosis

IV. Problems with the primary support group

V. Current GAF 57

There are myriad problems with this scheme. First, the use of the term

"axis" implies that each axis is independent from the others. Nothing

could be further from the truth. People with personality disorders,

for example, are more likely to have anxiety and depressive disorders

than others without personalty disorders.

Second, we don't really know what a "disorder" is. In most cases,

there is evidence of both psychosocial and biological causes for a

client's complaints. Both psychological and biological treatments are

effective for the same "disorders." So, what are we really treating?

Third, this scheme doesn't describe the quality of the client's life

very effectively, and that's what we really deal with in

psychotherapy. Axis IV, where this should be placed, is very general,

and poorly delineated. "Problems with the Primary Support Group,"

covers a lot of ground, from arguing with your wife to repeated sexual

abuse of a child.

Fourth, assessment of these disorders remains rooted in the clinical

interview. We've known since the 1950's, with a book by Paul Meehl

that clinical interviewing is not very reliable. Unfortunately,

psychologists, who are the true experts in assessment, have dropped

the ball entirely. We have not generated the kind of data necessary to

add psycosocial assessment to the diagnostic manual.

So, why do we need diagnosis at all? We need it to describe what we're

treating. We need it to organized our research into better treatment

methods. So as a result, we limp along with the diagnostic manuals as