3207902    สัมมนาการบูรณะความพิการแต่กำเนิด    Seminar On Congenital Defect Rehabilitation

การอภิปราย วิเคราะห์ และวิจารณ์ ความรู้จากวรรณกรรมเกี่ยวกับการดูแลรักษา บูรณะและติกตามผลผู้ป่วยที่มีความพิการแต่กำเนิด และพิการในระหว่างการพัฒนาการของร่างกาย การให้การรักษาปรับปรุง และแก้ไขปัญหาการออกเสียงที่ผิดปกติของผู้ป่วยประเภทนี้

(Discussion, analysis and criticism of the knowledge from literatures and textbooks about treatment, care, rehabilitation and maintenance of the patients with congenital deformities and developmental defects; treatment, improvement and correction of speech problems relared to these patients.)

(3207902 จุฬาลงกรณ์มหาวิทยาลัย)

Ma intreb de multe ori care este scopul meu, care e motivul meu, adevarul etc. Ma intreb de multe ori lucruri stupide carora nu le voi gasi niciodata un raspuns cert sau macar un raspuns. Astept in continuare ca dreptatea sa ne lege gandurile corect, intr-un final, sper in continuare ca cineva apoi inca cineva, apoi inca cineva, apoi toata omenirea va realiza anumite cusururi carora sa le si puna aplicare o rezolvare.

Tot citesc statusuri pe Y!M ca “In fata lui Dumnezeu suntem toti egali” sau “Dragostea e menita sa ne faca mai buni” ori fel si fel de prostii de genul, pe care, daca le-ar fi scris cineva mai in masura decat niste ipocriti, nu le-as fi judecat. Dar, asa, imi permit! Mi se pare absurd si aproape imoral sa faci pe Sfantul inca-Neproclamat in conditiile in care discriminezi, judeci pe nedrept, judeci dupa aparente, nu ierti, iti bati joc s.a.m.d. “Dumnezeu spune…”, dar tu faci?! De exemplu o tipa merge saptamanal la biserica, se roaga, pupa cruci si ce-o mai face, se considera o catolica smerita, insa inafara grupului crestin infatuarea, grosolania si nesimtirea sunt in floare. Cum sa nu deranjeze asa ceva? Oare chiar sunt eu nebuna? Or fi oamenii de acest tip prefacuti sau doar incapabili psihic?

Stiu ca probabil sunt rea si judec aspru si eu fiind imperfecta, ca toti restul, dar evit pe cat posibil nedreptatea pe principiul karmei sau…a constiintei(s-o numim asa). Ma rog. Inutil.

An eigfty year old woman, who had watched her father doing uzhichil, from the age of six, attended my sister who had a sprain.

She told my sister  that there will  be some defect in baby’s legs. These must be removed by pressing and shaking etc. of the portion affected, which only experienced family members are doing in Keralam. This way, shapely legs can be developed.

Normally it is neglected in modern life.

Calamity follies

The impact of the tsunami in Thailand and Indonesia, Bangladesh et al, Hurricane Katrina in the US, Typhoons Ondoy, Pepeng, Frank and Lupit in the Philippines reveals a pattern of serious defects in the political, economic, cultural, psycho-social institutions that direly need to be addressed in the present time without delay.

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My pregnancy with London was more eventful than either of my two previous pregnancies, to say the least.  I had morning sickness pretty much from the time I found out until my 13th week.  I did not have morning sickness with my other two pregnancies.  All was fine until my 24th week, when I started having contractions, which ended up being pre-term labor.  I was put on bedrest and was in and out of the doctor’s office with contractions.  After two months of bedrest, the doctors told me that I could now have the baby since I was 36 weeks.  Well, lo and behold, little London did not want to come out now.  I ended up being induced at 39 weeks.

    After 12 hours of labor and 3 pushes, London Max Mobley II entered the world at 8:01 p.m. on July 28, 2000 at Doctors Hospital in Manteca.  He had his umbilical cord wrapped around his neck twice.  He came through that ordeal just fine though, and as you can see in his pictures, he was a very pink and healthy looking baby.  He weighed in at 7 lbs 4 oz and was 20 inches long.  He had quite a bit of jet-black hair; we were quite surprised considering he comes from a family of bald babies on both sides!

He did wonderfully.  I had my tubes tied on Saturday July 29, 2000.  When I came out of surgery, we had a very hard time getting him to latch on to feed.  I insisted they give him a bottle, but the nurse (who was a wonderful nurse) knew of my wishes to give him no bottles, would not bring me a bottle.  She was as determined as I was that I was going to breastfeed.  But he would only latch on and feed for a few minutes and stop.

By Sunday morning, July 30th, I had noticed a considerable difference in his breathing.  When I pointed this out to the nurse, she attributed it to “newborn breathing.”  But I was sure this was not the case, my other two had the “newborn breathing” worked out after the first day.  And with his problems getting worse with latching on, this only made it worse.  Finally, breakfast came; I had just fed London for the few minutes he stayed latched on.  The nurse took him and told me to eat and not worry so much.  She then left the room, came back in shortly thereafter and said she was just going to take him to the nursery for a quick check.  I didn’t think too much of it since we were going home that day.  I ate my breakfast and waited, it seemed like forever.  London was never brought back to me.  I finally got up and walked out to the nursery, which was just down the hall.  What I saw when I looked in that window, I will never ever forget!  My son was lying on the table, clothes off, warmer on, chest leads on him and an oxygen tent over him.  He was getting bluer by the second.  The nurse asked me to come in and sit next to him.  Then I was called over by the on call pediatrician.  She said that they thought one of two things could be wrong with him, either he had a major infection known as sepsis or he had a heart problem.  Everyone there was pulling for the sepsis, not a great thing, but better than the latter.  They told me that they had called St Joseph’s Medical Center’s Transport team and that they were on their way to pick him up and take him to St Joseph’s in Stockton.  When they got there, they realized all they could do was try to get him stabilized and keep him that way.  They realized it was far worse than their hospital could handle.  So the Life Flight team from UC Davis in Sacramento was called.  About an hour later, he was on his way to UC Davis.  From what I was told, it only took them about 15 minutes to get up to UC Davis, whereas it took us about an hour to get there.  The whole way I was just a ball of tears.  The doctors told us that they pretty much knew what was wrong before the helicopter even got him there, all they had to do was an echo to confirm it when he got there.

We were taken right into a private conference room as soon as we arrived up at UC Davis.  We then were able to meet with the pediatric cardiologist, Dr. Michael Choy and the pediatric heart surgeon, Dr. Ralph Delius.  Dr. Delius had to leave, so we ended up talking to Dr. Choy.  He told us that London had HLHS.  He explained to us what that meant and told us of our three options.  We had to choose between a heart transplant, a three-staged surgery which consists of him having to have at least three open heart surgeries and our 3rd option, which was only an option for a split second, was compassionate care (we take him home and let him go).  London and I decided we had to give our baby every chance at life.  A heart transplant was just too risky in the fact that baby hearts are pretty hard to find.  So we chose the three surgeries.

On Wednesday, August 2nd, 2000 when he was only 5 days old, London went into his 1st open-heart surgery.  We were fortunate to have tons of friends and family with us in the waiting room to support us and help us through his surgery.  When he finally came out of surgery, we were relieved.  Now we just had to get through the first 24-48 hours.  These were the most critical they said.  Well, he made it through that.  And it was not too long before tubes and wires were coming out.

A little over a week after his surgery, he was moved from the Pediatric Intensive Care Unit (PICU) to the Continuing Care Nursery (CCN).  This was the last step before going home.  Well, lo and behold, that same night.  London started having heart arrhythmias.  We came in the next day expecting him to be fine, only to find in back in the Neonatal Intensive Care Nursery (NICU).  They had just given 2 medications to bring his heart rate down, but neither had worked.  They gave him the 3rd, Amiodarone.  It worked.  He was on Amiodarone and we spent another 4 weeks in the NICU.  As we were getting ready to go home a 2nd time, his heart rate started dipping really low.  They immediately took him off the Amiodarone and his heart rate went back to normal, then he had another arrhythmia, but this time his heart corrected itself on its own and it has never happened again.  We finally got to go home about a week later.

How scary it was to be taking home a sick baby.  Medicines round the clock, feedings every 3 hours on a feeding pump day & night, and on top of that, trying to pump about an hour before his feedings every time.  Not much sleep, let me tell you.  I mostly slept on the couch with him in his little bassinet right next to me and the feeding pump right next to him, always hooked up.  What a sight to see.

He did fine, except for the occasional blue spell, he would turn blue for no apparent reason, he did not stop breathing, just would turn blue.  Not very often though.  This was a cause of concern for the doctors.  So instead of waiting, they wanted to do his Glenn, the 2nd stage of open-heart surgery, on Feb 1st, 2001 when he was 6 months old.

We were fortunate to be able to take a trip the week before down to see my Grandmother, his Great Grandmother.  This was her 1st and unfortunately, her only time to see him (she passed away in October 2001).

February 29th, 2001 we headed up to UC Davis for his pre-catheter appointment and to stay at the Ronald McDonald house until his catheter the next day.  This went fine; so on Wednesday, February 1st they performed his Glenn.  He came through this one with flying colors.  He came off of the ventilator right away and completely off of oxygen early the next morning.  He had all but one IV and all catheters removed on Friday and Saturday.  His chest tubes and pacemaker were removed on Saturday afternoon.  We were moved from PICU to the Pediatric Ward on Sunday afternoon and we got to go home on Tuesday afternoon.

We ended up back in the hospital twice, once in March and again in April 2001, for a respiratory infection.  We could not figure out what was wrong, all tests came back negative.  The first time we were only in the hospital for 2 days and the last one, we were there for six days.  He ended up having Asthma, we have been able to keep it under control and have not been in the hospital for a “respiratory infection” since.

London turned 1 on July 28th, 2001.  He mastered crawling and climbing around the same time.  He weighed 18 lbs and was 29 inches tall.

On September 11th, 2001, London was scheduled for a heart catheter to coil some collateral’s he had growing.  We went in the day before for his pre-catheter appointment and found out that they had had problems scheduling it with pediatric anesthesia.  They needed anesthesia because they were going to have to go in through the neck.  So, needless to say, we were rescheduled for September 18th, 2001.  This was all not knowing what was actually in store for us on September 11th.  So, it turned out to be a good thing.  We were glad we weren’t up in the hospital away from our other 2 kids when the WTC was attacked.  We would have been freaking out!

He was having the heart catheter done because he had too many collaterals (extra veins growing between his heart and his lungs).  They had to go in and close them off with a special type of coil.  Something went wrong and one of the coils ended up in a vein that supplied blood to a part of the brain.  The object of the coil is to clot off and clog the vein so the vein will eventually die off.  This was not good.  They wanted to try to retrieve it.  If we left it alone, we risked him having a stroke and they did not know how bad it could be.  But if they went in to retrieve it, they could puncture the vein and case a stroke or worse, we could lose him.  They went ahead and tried to retrieve it, but were unable to.  The next 24-48 hours were crucial, we had to wait for his blood to clot to see what was going to happen.  Thankfully, he never had a stroke and so far as of today, has shown very minimal signs of any damage from the vein.

On January 10th, 2002, he had his 2nd heart catheter to finish coiling off his collaterals.  He had this one done at UCSF.  He came through it just fine.  It did take 6 hours, however they did not have to put him completely under this time.  They did have to put in over 30 coils though.  But the next day he was up walking around the halls!  We were released that afternoon.

Normally, they wait as long as they can to do the 3rd surgery, they like them to be about 45 lbs; he is now almost 23 lbs.  However, since he grew so many collateral’s, they don’t want this to happen again if they can help it, so the doctors want to do his 3rd surgery in about a year, which is sooner than we were expecting.  Usually, they end up doing it around 3-5 years of age.

Revision C of the Project Mindwell toxicological presentation on Mercury (Hg) is now released:
- http://www.scribd.com/doc/21321125/Mindwell-Mercury-An-Overview-of-this-Toxin-Rev-C

This revision was just a format update to make it a bit cleaner and in line with other Mindwell documents.

Pass it around!

Nu am incercat niciodata sa ma gandesc la scris. Am luat acest lucru de la bun inceput, ca pe un lucru la care nu sunt foarte buna. Dar incapatanata fiind, nu ma las usor.
De fapt ce vreau sa spun, nu este legat ,neparat, de mine … am dat un exemplu .

Pe acest mare world wide web sunt mii si mii de pagini ale unor persoane ce isi descarca frustarile, visele, isi plang iubirile pierdute, isi canta povestea de dragoste, se dau cu pararea, nu se dau cu pararea, pur si simplu scriu sau scriu doar doar poate devin si ei/ele “famous”. Sunt 3 categorii mari : oameni ce au ceva de spus dar o fac prost, oameni ce nu au nimic de spus (povestesc despre ce tare e iubitul, despre cat de nasola fost iubitul, despre prietena cea mai buna, despre rautatea si bunatatea din lume) ( “nimic de spus”=lucruri atat de banale si generale “) , acest nimic ce defapt este o generalitate asupra lumii care poate fi supsa in acelasi mod si de un copil de 5 ani. Si da, ati ghiciiiit, mai am o categorie : cea a sarcasticilor: o combinatie intre lucruri inteligente de spus si umor (uuuuuu….asta e favorita mea).

Dupa cum vezi nu ma deranjeaza faptul ca ceea ce spun/scriu ar avea o calitate prosta, fiecare are ceva de spus….ma deranjeaza catergoria intermediara care dau impresia ca spun ceva cand defapt ceea ce spun este egat cu nimic, pentru ca e pur si simplu un general valabil . Sa dau exemple?@?@
ok…uite un exemplu
…
” in viata te vei lovi cu capul, in viata te maturizezi odata cu acumularea de experiente, fie bune fie rele, te vei lovi, te vei ridica si daca ramai pozitiv vei reusi”…asa arata cineva care vrea sa dea impresia ca spune ceva.
…
“trec repde de la un subiect la altul, imi place sa ma imbrac cochet, toti prieteni mei sunt prietenii mei, pana si bunica…sunt vesela, ba sunt trista, sunt vesela, sunt trista, ….”

Dar in cele din urma cu totii suntem liberi sa facem absolut tot ce vrem, si cine sunt eu sa spun ce e bine si ce nu…Ehhh…am dat-o si eu un pic cu barfa acum ))))

Hai sa lasam cantitatea si sa ne vandim la calitate.

During a small group (round table) meeting in Quezon City at the residence of poet and writer Rolly Carbonell, Author, poet,on forthcoming hazards from climate change and the solar super storm in 2012-2013, everyone shared their their ideas on various psycho-social issues that need to be considered about this event in the near future.

Initially, the group discussed the impact of the tsunami in Thailand and Indonesia, Bangladesh et al, Hurricane Katrina in the US, Typhoon Ondoy in the Philippines.

The Convenor of the conference, Sen. Edgar U. Ilarde, said that there will even be bigger catastrophes come 2012 and 2013, when the phenomenon of the solar climax or solar maximum takes place.  This will be in the form of a magnetic storm or a solar super storm that has devastating effects on both humans and more potently upon satellites, electronics, communications and many other devices powered by electricity.

On the other hand, Author, poet, philosopher George Sison, said:

The way we approach disaster, those in the past and especially those that are forthcoming, it almost looks like we brought these things upon ourselves.

George was saying that as if by mute agreement, we all collectively invoke disaster and will calamities to wreak damage upon ourselves and loved ones. Our conventional conscious acts and thinking either make or help make storms and earthquakes to happen. This is a dangerous thing to do. Psychically inviting peril and death.

George was also saying that we, as a people that are called Filipinos, are the only ethnic group that apparently suffer from negative karmic vibrations that in selected places of the world, once identified as Filipinos, we are discriminated against.  In George’s experience, he says he was extremely humiliated in an airport when someone asked who were from the Philippines and segregated all those that raised their hands from  the rest and told to occupy a corner so as to be processed longer than the rest of the travelers.

Such negative karma in a collective, George says, if powerful enough can also be contributory to events that happen in the environment. Together with the negative psychic energy of many others in the rest of the planet, we could even trigger bigger, much more tremendously powerful calamities all around the world.

More about this post here.

I updated the Mindwell: Toxicology on Fluoride / Fluorine (F) PDF to include another good chunk of information from a different source and I updated the layout dramatically.  Please download and use the new (Rev. B) version of the document!

LINK: http://www.scribd.com/doc/21720313/Mindwell-Fluoride-an-Overview-of-This-Toxin-Rev-B

Yesterday afternoon I was processing my photos from my trip to Immigration using Adobe Photoshop Lightroom 2.4. I was using my normal multi-pass workflow which has worked well for me.

Lunch!

I was in Library Loupe mode about to enter a title and caption to this photo about my lunch at Delifrance.

Then Lightroom stopped working.

When I clicked on it the title bar changed from its normal black to blue (Adobe must do some Windows user interface funnies to get that black colour) but that’s all it would do.

Lightroom was not consuming much CPU and I was able to take this screen shot when I decided it was never going to talk to me again. It was not a particularly large shoot – only about 100 pictures. It has handled several times this number without a problem in the past.

I have plenty of disk space and 2GB of memory. I guess it ran out of some resource.

I terminated the process, restarted Lightroom and did a catalog database check, backup and optimize. Lightroom is back to normal now but I am worried the catalog is corrupted in some way. Desktop databases typically do not like it when you terminate their process before they have had a chance to post their buffers. This isn’t Oracle or DB/2!

I checked that the previous photo I had modified had its data as I expected it.

Are there any other tools I can use to check the catalog? I don’t want to be using a catalog that has problems and will fail more seriously.

Maybe unfairly I tend to blame MS Windows. This is the kind of thing that makes me want to follow Jeff Friedel, ditch the ball and chain and escape Windows.

You just want to stare,
but no matter how hard
you try you can’t help
Looking.
Surely it’d be
More polite to comment
Or the birth mark or
disfigurement.
Complementing on it’s
Unique angle. Or inspired
Use of colour.
But they know,
it’s not as if you
are the first to stare.

Here is a breakdown / general overview of the Toxin: Fluoride / Fluorine(F)

LINK: http://www.scribd.com/doc/21720313/Mindwell-Fluoride-an-Overview-of-This-Toxin-Rev-A

======================================================

FLUORIDE 

10.1                  INTRODUCTION 

• …high levels of waterborne F are also hazardous to both human and animal health. For example, in China and India millions of people are suffering from dental and skeletal fluorosis – abnormal or poisoned tooth and bone conditions induced by F – mainly due to consumption of high levels of F in drinking water.

 10.2.5               FOODS 

• F intake from food and beverages by a male residing in a fluoridated community in the U.S. is about 1 to 3 mg/day. It is decreased to 1.0 mg/day in a nonfluoridated area.  The intake from drinking water ranges from 0.1 to 0.5 mg/day in nonfluoridated communities, whereas in fluoridated communities it may amount to 1 to 2 mg/day. 
• Several plant species are known as F accumulators. Examples include camellia (620 ppm), tea (leaves, 760 ppm), and elderberry (3600 ppm, dry basis). 

10.3                  INDUSTRIAL SOURCES OF FLUORIDE POLLUTION

10.3.2               MANUFACTURE OF PHOSPHATE FERTILIZERS 

• In the aqueous scrubber, SiF4 readily reacts with water, forming fluorosilicic acid (H2SiF6), as shown in Reaction 10.3. Fluorosilicic acid is highly soluble in water and is readily absorbed by plants. 

10.3.3               MANUFACTURE OF ALUMINUM 

• A number of other substances are emitted in the process. This is because several catalysts, including CaF2, AlF3, and cryolite, are used in the eletrolysis of alumina, and as these are heated at high temperatures, some will escape from the cells, contaminating the surrounding atmosphere. 
• …several other gases, including SO2, SiF4, HF, COS, CS2, He, and water vapor, are also produced… 
• Moreover, a large number of particulates are also emitted, including Al2O3, carbon (C), cryolite, AlF3, CaF2, Fe2 O3, and chiolite (Na5Al3F14). 

10.3.4               MANUFACTURE OF STEEL 

• In the manufacture of steel, calcium fluoride (CaF2) is used as a flux… F compounds emitted from this operation include HF and CaF2. 

10.3.5               COMBUSTION OF COAL 

• As mentioned previously, coals mined in U.S. contain about 0.001 to 0.048% F, usually as fluorapatite or fluorspar. Combustion of coal in power plants, therefore, emits considerable quantities of F into the atmosphere. During combustion, about half of the F in coal is emitted as gaseous HF and SiF4 and particulate matter. 
• For example, studies show that several cities in China, including Chongqing and Beijing, are experiencing severe fluoride air pollution problems arising mostly from coal combustion. 
• Another important source of F in Beijing is dust from fresh concrete used for construction. 
• Fluoride has also been traced to runoff from application of insecticides and herbicides. 

10.4                  EFFECTS ON PLANTS 

• HF is the most phytotoxic air pollutant. 
• F accumulates in the foliage of plants. The plants then serve as a vehicle for transfer of F to herbivores, with the potential for inducing dental and skeletal fluorosis. 

10.5                  EFFECTS ON ANIMALS 

10.5.1               INTRODUCTION 

• Animals normally ingest small amounts of F in their rations without observable adverse effects, but excessive intake can be detrimental. 

10.5.3               CHRONIC EFFECTS 

• The two most conspicuous and thoroughly studied manifestations of chronic F poisoning are dental and skeletal fluorosis. Once absorbed into animal body, F has a great affinity for developing and mineralizing teeth. This affinity can either enhance tooth development or induce dental lesions, depending on the amounts of fluorides ingested. 
• Furthermore, it is often found that F levels are inversely related to the distance between the industrial facilities and the site of animal collection. 
• Lameness or stiffness is an intermittent sign of F toxicity. … The clinical basis for the lameness is not well understood. 

10.6                  EFFECTS ON HUMANS 

10.6.1               DAILY INTAKE 

• Daily intake of F by individuals in the U.S. is about 0.2 to 0.3 mg from food, 0.1 to 0.5 mg from water (1 to 2 mg if water is fluoridated), and varying quantities from beverages (F content of wine is 0 to 6.3 ppm, beer contains 0.15 to 0.86 ppm, and milk, 0.04 to 0.55 ppm). The amount of F inhaled from air is about 0.05 mg/day. 
  • NOTE: Toothpaste not mentioned (1 or 2 times daily), dermal contact and inhalation during showering / bathing / swimming is also not mentioned.
  • There is approximately 1,000 ppm F in toothpaste and approximately 0.22 ppm F is actually ingested by a 5 year old child per brushing.  This does not include what remains in the mouth when done / rinsed.
    • http://www.fluoridealert.org/f-concentrations.data.htm#tp
  • Soda usually contains approximately 0.60 ppm F, infant formula, processed cereals, juice, cigarettes, and fluoridated salt are other sources.
    • http://www.fluoridealert.org/f-sources.htm 

10.6.2               ABSORPTION 

• Absorption of F from the gastrointestinal tract occurs through a passive process; it does not involve active transport.1 Absorption is rapid and probably occurs in the lumen. The rate of absorption is dependent on the F compounds involved, e.g., 97% of NaF, 87% of Ca10F2(PO4)6, 77% Na3AlF6, and 62% CaF2 are absorbed. About 50% of the absorbed F is excreted by the kidneys while the remainder is stored, primarily in calcified tissues. 
• Even at low levels of F intake, appreciable levels of F will, in time, accumulate in calcified tissues. 

10.6.3               ACUTE EFFECTS 

• The lethal dose of inorganic F has been estimated to be in the range of 2.5 to 5 g for a 70 kg male… 

10.6.4               CHRONIC EFFECTS 

• Fluoride accumulates in the skeleton during prolonged, high-level exposures. Radiological evidence shows hypermineralization (osteofluorosis) occurs when bone F concentrations reach about 5000 ppm. 
• Fluoride exposure leads to cell damage and induces necrosis. Eventually, F produces massive impairment in the functions of vital organs, particularly when given orally. 
• Airborne F from the combustion of coal was found to pollute extensively both the living environment and the food, such as corn, chilies, and potatoes, that the residents consume. 
• Several groups of researchers have reported reproductive effects of F in humans. 
• Levels of reproductive hormones were also measured; the High Fluoride Exposure Group showed higher follicle stimulating hormone but lower inhibibin-B, prolactin, and free testosterone serum concentrations than the Low Fluoride Exposure Group. 

10.7                  BIOCHEMICAL EFFECT 

10.7.2               IN ANIMALS AND HUMANS 

• F inhibits the metabolism of carbohydrates, lipids, and proteins. In animals and humans, a large number of enzymes are depressed by F, including enolase, ATPase, lipase, and cholinesterase. Inhibition of glycolysis, due in part to decreased enolase activity, may be responsible for the hyperglycemia observed in laboratory animals exposed to F. 
• F stimulates adenylcyclase activity in all tissues so far examined… 
  • From Wikipedia: In neurons, calcium-sensitive adenylate cyclases are located next to calcium ion channels for faster reaction to Ca2+ influx; they are suspected of playing an important role in learning processes. This is supported by the fact that adenylate cyclases are coincidence detectors, meaning that they are activated only by several different signals occurring together.
    • http://en.wikipedia.org/wiki/Adenylate_cyclase  
• F also affects functions controlled by Ca in humans, as it does in plants. These functions include blood clotting, membrane permeability, and cholinesterase activity. 
• In the presence of F, Mg2þ and MgADP form a complex MgADP– MgFx that traps the active site of S1 and inhibits myosin ATPase.  As previously mentioned, F is shown to inhibit protective enzymes, such as SOD, glutathione peroxidase (GSHPx), and catalase, in various human tissues.  Inhibition of one or more of these enzymes may allow free-radical-induced reactions to occur, leading to cellular and tissue damages. 

10.8                  NUTRITIONAL FACTORS AFFECTING FLUORIDE TOXICITY 

• … several nutrients have been shown to alleviate injuries caused by exposure to F.  The nutrients studied so far include proteins and Ca, and vitamins C (ascorbic acid), D, and E. Glutathione (GSH), which is not a nutrient but a well-known antioxidant, has also been studied. 
• …F-treated chicks showed a marked decrease in ascorbic acid levels in the heart, spleen, brain, gizzard, and pancreas, while the levels were increased in the lungs and kidneys. 
• Results showed marked decline of ascorbic acid in adrenal glands and kidneys in the F-treated cockerels. Furthermore, the levels of DHA in the kidneys of the F-exposed cockerels increased more than 100% compared with the control levels. 
• In laboratory mice, both protein and vitamin C were shown to lower F accumulation in bone. For example, mice fed a low-protein diet (containing 4% protein) supplemented with 150 ppm NaF deposited five times more F in the tibia than did control mice fed a regular diet (containing 27% protein) and exposed to the same level of NaF. Furthermore, supplemental vitamin C greatly lowered F deposition in the bone.34 (It should be noted that mice also produce vitamin C.) 
• Fluoride treatment has been shown to induce embryotoxicity in pregnant rats. … A higher incidence of skeletal and visceral abnormalities (subcutaneous hemorrhage) was observed in the fetuses of the F-treated pregnant rats. Oral administration of vitamin C (50 mg/kg body weight) with NaF significantly reduced the severity and incidence of F-induced embryotoxicity in the rats. 
• Exposure of male mice to NaF (10 mg/kg body weight) for 30 days showed a marked decrease in cauda epididymal sperm count, motility, and viability, resulting in significant reduction in fertility rate.  Withdrawal of NaF treatment for 30 days produced incomplete recovery. However, when vitamin E or vitamin D was supplemented during the withdrawal period, the toxic effect of NaF was significantly alleviated, as the treated mice restored their reproductive functions and fertility. Additionally, it was found that a combined administration of vitamins D and E was generally more effective than either vitamin D or E administered alone. 

ENVIRONMENTAL TOXICOLOGY – Second Edition
Biological and Health Effects of Pollutants
Ming-Ho Yu
ISBN: 1-56670-670-X

 ============================================

 J Toxicol Environ Health. 1994 May;42(1):109-21.

Exposure to high fluoride concentrations in drinking water is associated with decreased birth rates.

Division of Biometry and Risk Assessment, National Center for Toxicological Research, Jefferson, Arkansas 72079.

A review of fluoride toxicity showed decreased fertility in most animal species studied. The current study was to see whether fluoride would also affect human birth rates. A U.S. database of drinking water systems was used to identify index counties with water systems reporting fluoride levels of at least 3 ppm. These and adjacent counties were grouped in 30 regions spread over 9 states. For each county, two conceptionally different exposure measures were defined, and the annual total fertility rate (TFR) for women in the age range 10-49 yr was calculated for the period 1970-1988. For each region separately, the annual TFR was regressed on the fluoride measure and sociodemographic covariables. Most regions showed an association of decreasing TFR with increasing fluoride levels. Meta-analysis of the region-specific results confirmed that the combined result was a negative TFR/fluoride association with a consensus combined p value of .0002-.0004, depending on the analytical scenario. There is no evidence that this outcome resulted from selection bias, inaccurate data, or improper analytical methods. However, the study is one that used population means rather than data on individual women. Whether or not the fluoride effect on the fertility rate found at the county level also applies to individual women remains to be investigated.

PMID: 8169995 [PubMed - indexed for MEDLINE]

==================================================

 Fluoride 1994; 27(1): 7-12 

Effect of Fluoride on Rat Testicular Steroidogenesis – Narayana MV, Chinoy NJ 

ABSTRACT: In view of reports of infertility among human populations in fluorosis prevailing regions, we investigated the effect of fluoride ingestion on testicular steroidogenesis in rats. Sodium fluoride (NaF) was administered to the rats orally at a daily dose of 10mg/kg bodyweight for 50 days. The treatment did not cause significant change in testicular cholesterol levels, indicating that metabolism was not altered and that there was no hypo/hypercholesterolemic effect. In addition, activities of the intermediary enzymes in androgenesis, viz., 3ß- and 17ß-hydroxysteroid dehydrogenase were only modestly decreased by NaF ingestion. Subsequently, the determination of circulating androgen levels was similar in NaF-treated rats showed a downward trend compared to those of the control group, suggesting alteration in testosterone concentration. The histomorphometric studies revealed significant change in the Leydig cell diameter m correlation with the androgen levels. These results indicate that fluoride does interfere with steroidogenesis in short-term lowdose exposures in rats.

Canon just issued a service notice for the new EOS-7D. It says that under “certain conditions” (unspecified) in continuous shooting mode slight traces of the previous image may appear on a subsequent image. They apologised profusely and promised a firmware update to fix the problem.

Here is a link to the service notice (USA).

Camera firmware is getting so complex now that this kind of bug will appear more often from all manufacturers. I think software QC still trails hardware by miles.

Of course, as a Frugal Photographer I am delighted at the news. Another reason why I can tell myself I shouldn’t buy this camera that I crave!

If a man does not keep pace with his companions, perhaps it is because he hears a different drummer. Let him step to the music which he hears, however measured or far away.

— Henry David Thoreau

In “The New Untouchables “, New York Times columnist Thomas Friedman argues that in this downwardly mobile economy there is no room for average. Extraordinary is what it takes to survive and thrive in the modern workplace.

I get that.

Yet for all my appreciation for education — I hold two degrees so I do, in fact, lean in favor of Friedman’s premise that education is key to American competitiveness — his education-as-a-panacea argument oversteps its reach.

Most strikingly, Friedman’s description of a successful “untouchable” American worker isn’t a portrait of educational endowment at all. Friedman’s favorite descriptors, instead, refer to personality attributes: entrepreneur (risk taker), creative (visionary), analytical (critical thinker), and persuasive (charismatic). The obvious problem with Friedman’s pin-the-tail-on-the-wrong-donkey premise is that temperament is inborn — teachers, let alone parents, cannot instill personality characteristics that are not there to begin with.

Friedman’s eagerness to finger the usual suspects — schools — also ignores six reasons why Americans are at a competitive disadvantage in the global era. Here we examine those realities, and the future these changing times have in store.

First, there are more of us occupying this country — and this planet at large — than ever before. At some point, the mathematics of population growth have to matter. The sheer number of people in today’s workforce suggests more and more people are competing for the same jobs even as we adopt more and more technology to displace human hands. That’s not a sign of a lack of education; it’s a sign that business owners comprehend that productivity gadgets and gizmos don’t require breaks, a salary or workers’ compensation.

It comes down to the numbers.

Second, I would argue the inverse in response to Friedman’s suggestion that there just isn’t enough talent to be had here in the States. Over the past 50-some years there are more colleges turning out more graduates on an annual basis than employers of the past had access to. Many foreign nationals, in fact, come to the US for higher education opportunities. On the flip side, there are only so many engineers, M.B.A.s, lawyers, scientists and the like universities can churn out before higher-end fields become saturated in much the same way low-end jobs are chalk full of contenders.

It’s no longer merely a question of whether there are clear winners and losers on the academic front.

Job scarcity is a threat, in part, because of the decades-long trend of mergers, acquisitions and a globalized labor pool. Consider: There are generally fewer than a dozen heavyweights in a given industry — everything from mainstream media to appliance manufacturing. This trend does not bode well for domestic job expansion. And if jobs aren’t available to begin with, it is tough to gain a competitive advantage even with above-average potential. So what we are seeing, in this author’s opinion, is an over-supply of talent.

But that doesn’t mean the proponents of Friedman’s dire self-fulfilling prophecy won’t get their wish.

With less competition in a given industry there is less demand for the eager young grads institutions of higher learning infuse into the job market each year. With shrinking demand and a greater supply of contenders, salaries may also take a nosedive. America at large may become competitively disadvantaged in the years ahead precisely because the “good jobs” of today are no longer perceived as a source of steady employment or adequate pay thereby diminishing American college students’ willingness to pursue them.

Already, the very cure that causes the “employment insecurity” disease is well underway: Calls for immigration reform permitting more foreign grads to take up permanent residence in the U.S. as a form of “insourced talent” are originating from Google, Microsoft and Susan Hockfield, MIT president and author of an October 19, 2009 Wall Street Journal opinion piece ironically titled “Immigrants Create Jobs and Win Nobels“.

Sure there are a lot of average people who aren’t cut out for the highest levels of business, government and academia. Just the same, there is also an ample supply of bright, talented American citizens who, for all their desirable qualifications and qualities, will nevertheless find themselves competing toe-to-toe against peers who are just as capable and “deserving” of a career break as they are.

Somebody has to lose.

Third, failure to thrive in this Brave New Economy isn’t always linked to failing schools, as Friedman argues. Good health is arguably the number one prerequisite to productivity. Healthcare is such a hot topic precisely because we cannot remain competitive if, as a country, businesses and individuals are increasingly diverting money out of the real economy just to keep up with the skyrocketing cost of healthcare.

Beyond that, few esoteric explanations matter when perfectly down-to-earth explanations suffice. When an individual charged with hiring decisions has too many promising applicants to choose from among, what assets wins out on the last round of interviews? That extra year or two of experience? Those additional GPA points? Or would it be more honest to conclude that it comes down to how well an applicant clicks with his or her interviewers? Hands-on experience, even a social or physical attribute — whatever it may be that fits a manager’s self-styled view of the proper candidate — is just as likely to make the deciding difference.

On the flip side of the coin, there is a perverse disincentive to hire the best qualified candidates. For one, they tend to be more experienced and/or highly educated, thereby commanding greater salaries. For another, few people in the position to do so hire individuals with the obvious capacity to perform so impressively that it will ultimately threaten their own job security. Friedman is right in the sense that education and talent ought to insulate Americans from the pitfalls of a failing global experiment.

Unfortunately, it does not.

Fourth, where one lives also figures largely into one’s ability to compete. Like the tough-luck stories that abound on the streets of Hollywood, those who flock to saturated markets — Los Angeles, New York, etc. — may, ironically, find fewer opportunities to leave a lasting, positive impression due to the sheer number of people in the area who are equally worthy of consideration. An over-supply of applicants for a given position, in turn, may make it more challenging for employers to select optimal talent vs. expedient talent. Translation? Being a big fish in a vast ocean still makes you a little fish. To argue, therefore, that education can somehow imbue success and that lack of it underlies a failure is a misnomer.

It’s impossible to underestimate the economics of supply and demand.

Fifth, it’s a mistake to assume that a Third World factory worker is more “competitive” as Todd Martin, former PepsiCo and Kraft Europe executive, suggests to Friedman. Third World workers come inexpensively, and that’s one competitive disadvantage that will only heighten the more educated the American workforce becomes. Why? Because talent doesn’t come cheaply — nor do the salaries of increasingly educated job seekers struggling to repay oppressive student loan debts as a direct result of their herculean efforts to rise head-and-shoulders above the crowd.

Getting noticed in an increasingly competitive job market only ups the ante — and the price tag of success.

Sixth, the assumption that Third World products are better made by virtue of their “efficiency” is also flawed. When frequent replacements and upgrades are factored into the cost of ownership, inexpensively manufactured Third World goods are, ironically, quite pricey. Case-in-point: In 2005 I replaced a 30-some-year-old GE refrigerator made in the US as well as an old but functioning washer and dryer. If I had to do it all over again, I wouldn’t trade anything old and working for something new, sleek and modern. Why? Because the major appliances I purchased new in 2005 — all have had repeated major breakdowns requiring multiple service calls, dozens of hours on the phone, weeks waiting for parts.

Even when consumers spend top dollar, the manufacturing source and quality of today’s big-ticket items are often quite similar — with merely a change of window dressing to imply otherwise. That’s what happens when there are so many market consolidations that an appearance of choice is just that: little more than a dozen or so name badges owned, in truth, by the same handful of Big Players. It is almost laughable the degree to which consumers on complaint websites proclaim that they will never buy brand “X” again, only to unwittingly state that they intend to replace such-and-such item with brand “Y” — yet another brand or subsidiary of the very same company who manufactures brand X!

Market concentration doesn’t grow jobs any more reliably than it promotes healthy competition.

Sparing one another the hassle and headaches of poor quality goods isn’t the only reason to care, however. The build-it-to-last ethic of decades past was, perhaps, the ultimate expression of “Green“. Why? Because durable goods were seemingly less likely to break down, destined for a landfill in an absurdly short timeframe. By contrast, “planned obsolescence” is the new norm, with a trend of shrinking manufacturer warranties to attest to the low vote of confidence manufacturers assign to their own products. Longevity isn’t a valued trait in a disposable society, but if we really want to go Green perhaps we should rethink the “dept-trap consumerism” cheaply designed and manufactured products facilitate. Sadly, modern rhetoric would have us believe that pride in one’s workmanship — a refusal to sell junk to unsuspecting consumers — is “uncompetitive”.

All talk of going Green aside, standardized manufacturing processes have made it difficult to make the case that company “A” is making a better product than “B” or “C”. Consequently, the maxim “You get what you pay for” has never been more suspect. True, you may get more for your money, but that does not necessarily translate into significantly better quality. What differs most dramatically is the amount of money corporations throw into slick ad campaigns, and the perception consumers have of branding and value.

It would be one thing if high-end boutiques were selling products made by First World craftspeople with higher price tags thanks to First World production costs. But when both low-end retailers and high-end retailers are selling inexpensively made foreign goods, who, exactly, are they fooling? Fairly or not, Third World origination suggests that income and human rights disparities favor corporate bottom lines. In the Third World, after all, it is not uncommon for workers to be denied bathroom breaks, sick days, maternity leave and most of the other benefits and protections Americans consider “civilized”. It is not surprising, then, that workers are more productive when they spend most of their lives in the confines of a factory, fearful that their only other option is a life of abject poverty and/or prostitution.

In short, the Third World is the modern-day economic equivalent of the pre-Civil War Old South: a place for slave-like child and adult labor, often conducted under sweatshop conditions. As if that weren’t questionable enough, outsourcing trends pose an unacceptable risk to national security as well.

So how does all of this tie in?

Unless Americans are willing to stoop to similar lows to compete with workers abroad, it’s not possible to rationally conclude that education, talent or entrepreneurship on the part of American workers will level the economic playing field anytime soon. America’s competitive disadvantage, rather, speaks to corporate opportunism — and to the politicians in recent decades who have crafted immigration, economic, trade and taxation policies that have enabled such heavily skewed commerce to become the norm.

Moreover, if being properly educated, creative or analytical adequately described, as Friedman suggests, the entirety of American competitiveness, I suspect we would see fewer reckless gambles on Wall Street and more evidence of long-range thinkers putting the brakes on short-term gain (scams) in the lead up to the Great Recession. In the real world, however, the “right reasons” are not always the cause for getting ahead — or, conversely, for falling behind.

THE WAKE UP CALL

So why care whether or not a newspaper columnists gets it so wrong? Because generalizations and simplifications aren’t a starting point for progress. Economists are projecting a ~10 percent national unemployment rate that’s here to stay for the foreseeable future. That can only mean more bankruptcies, more foreclosures and a greater amount of “dead weight” on America’s ability to compete. Only by taking a long, hard look at the unvarnished truth do we have any hope of fingering the right culprits, crafting the right solutions and ultimately reviving Main Street before the American Dream becomes a distant memory of a bygone era.

Doing nothing is not an option.

If Middle Class wages continue to decline as we move further into the 21st Century, who will consume the products and services entrepreneurs on both sides of the oceanic divide offer? Will young Americans, contemplating the grimness of their economic future and/or the need for ever-more costly and impressive academic résumés opt for traditional marriage and family life — the nation’s greatest driver of new purchases, everything from strollers and diapers to single family homes and minivans? Should Main Street’s economic House of Cards continue to crumble, will Third World workers have their own Friedmans urging them to blame themselves when factory orders dwindle and the newly affluent in Asia and India begin to see their own hopes and dreams falter? Or will they see it — we see it — for what it is: globalized economic forces beyond any single individual’s immediate control?

As kind-hearted as sweatshop proponents paint it — that throwing out more life preservers will rescue Third World residents from a life of “primitive agriculture” — building more life preservers than boats is a plausible scenario. Economic growth, after all, relies on expansion. For much of the world’s history markets were local, national, then regional. Globalization isn’t a sure-fire path to success: It’s an experiment that presupposes that natural resources will support endless growth. And it begs a simple but profound question: What happens when all markets are tapped out?

Working and Middle Class people — the majority of us — may not be the most educated, creative or adequately prepared lot, to hear Friedman and his corporate pal, Todd Martin, hash it out. But that doesn’t change the reality that the American Middle Class must earn a living wage in order for the economy — ours and theirs — to thrive. Yet it is telling that in Louisiana, a state with fewer college grads to begin with, Curt Eysink, director of the Louisiana Workforce Commission, indicates that there is an oversupply of degreed residents “we cannot employ” because job growth projections favor vocational trades and the service sector — primarily low-wage occupations such as ticket-takers, cashiers and customer service representatives that are not so prone to the insourcing/outsourcing phenomena.

Is this a sign of things to come?

Without the discretionary income Middle Class Joes and Janes inject into the marketplace, globalized economies may become relegated to a small percentage of elite income earners pitching their products and services to other elite individuals. This may be a recipe for modern-day feudalism, but it’s no way to protect and preserve the merits of free-market capitalism, let alone a profitable market share.

As dire as it all sounds, this isn’t about being pessimistic. Opening our collective eyes is the first step in defending what matters most: family, community, culture — the United States itself. If that means rethinking our definition of progress in the 21st Century sans the usual set of partisan blinders, so be it.

This is no time for subterfuge.

If Friedman wishes to talk about education, he ought to contemplate the wisdom no book learning apparently can impart in America’s best and brightest CEOs and newspaper columnists: The foresight to realize one’s employees/coworkers are also one’s customers/consumers. That means that success at the top of the economic pyramid is only as long-lived as the Middle Class foundation upon which it rests. Excuse it, deny it, defend it, ignore it: the race to the bottom is a very real risk when good intentions go too far.

It’s foolhardy — and a threat to democracy itself — for a transnational conglomerate, an economy, a nation, to conduct business using the lowest common denominator as a competitive yardstick. And yet, globalization promises to outsource gain even as it insources pain. At best, this implies that if and when international economic and trade equilibrium is achieved Third World laborers will nevertheless be unable to sustain the lifestyle Americans have taken for granted — if only by virtue of how thin finite natural resources are stretched — whereas Americans should anticipate “economic insecurity” as a way of life. That’s why Friedman and friends argue so passionately that being wildly successful — untouchable thanks to one’s creativity, innovativeness and education — is the only position of safety (familiarity). The rest of us, apparently, are destined for a mediocre economic melting pot in a neocapitalist New World Order.

Cliché though it may sound, the proactive response to an uncertain future is civic engagement: voting wisely with one’s ballot and one’s pocketbook in support the kind of economy one wishes to see. For if there’s any silver lining to this Great Recession, it’s in bringing an abstract global issue close enough to home that we can reach out, touch it — and change it.

It’s not too late.

###

Resources:

America Out of Work: Is Double-Digit Unemployment Here to Stay?/TIME

Obama Adviser Summers Rejects ‘New Normal’ of Slow U.S. Growth/Bloomberg

U.S. Job Seekers Exceed Openings by Record Ratio/NYT

Are You Prepared for a Jobs Depression?/ere.net

How Long will America Lead the World?/Newsweek

Cap and Trade Dementia/The American Spectator

Schools As Scapegoats/The American Prospect

Is it Time to Retrain Business Schools?/NYT

Go Global, Young Manager!/Financial Post

Is a College Degree Worthless?/MSN Money

Don’t Get That College Degree!/NY Post

Cat Gets GED: Why GPAs, Degrees and Job Titles May Be Worthless/ITBusinessEdge

Too Many Doctorates Chase Too Few Jobs/San Francisco Chronical

The Three-Year Solution/Newsweek

Asking for Student Loan Forgiveness/Businessweek

Middle Class Facing Decline in Expectations, Economic Power/Retail Traffic

21st Century Skills, Education & Competitiveness/PDF

Jay Mathews: Why I don’t Like 21st Century Reports/Washington Post

Friedman: U.S. Education System Endangering Global Competitiveness/Education Futures

A New Look at American Competitiveness/Entrepreneurship

The World’s New Superpower/Salon

The Almighty Renminbi?/NYT

The End of the Dollar Spells the Rise of a New Order/The Independent (UK)

China will Overtake America, the Only Question is When/The Independent (UK)

China’s Economy/Brookings Institution

Lax Oversight, Globalization Erode Product Safety/CNN

Technology Made to be Broken/CSMonitor

Appliance Anxiety — Replace It or Fix It?/NYT

I updated the Mindwell: Toxicology on Mercury PDF to include another good chunk of information from a different source.  Please download and use the new (Rev. B) version of the document!

LINK: http://www.scribd.com/doc/21321125/Mindwell-Mercury-An-Overview-of-this-Toxin-Rev-B

Here is a breakdown / general overview of the Toxin: Mercury (Hg)

Here is the Scribd Link: http://www.scribd.com/doc/21321125/Mindwell-Mercury-An-Overview-of-this-Toxin-Rev-A

MERCURY

12.4.1               INTRODUCTION

• “Hg has no known biological role and, because of its diversity of usage, is an industrial health hazard. It is a bioaccumulative metal that is fat soluble, and has many damaging effects on living organisms.” (12.4.1)

12.4.3               SOURCES OF MERCURY POLLUTION

• “The majority of Hg comes from anthropogenic sources. Mining, combustion of fossil fuels (Hg content of coal is about 1 ppm), transporting Hg ores, processing pulp and paper, incineration, use of Hg compounds as seed dressings in agriculture, and emissions from smelters are some examples. In addition, Hg waste is produced as a by-product of chlorine manufacturing plants and gold recovery processes, and is found in used batteries and light bulbs.” (12.4.3)

12.4.5.3            EFFECTS OF MERCURY ON ANIMALS

• “Fish may accumulate Hg in excess of the 0.5 mg/g FDA guideline.” (12.4.5.3)

• “Because increased temperature enhances metabolic rate, more Hg is concentrated in the summer than in the winter. The toxicity of Hg and other heavy metals to fish also increases with an increase in temperature.” (12.4.5.3)

• “Wild birds concentrate the highest levels of Hg in the kidney and liver, with less in the muscle tissues. … Many species of birds declined, both in numbers and in breeding success…” (12.4.5.3)

• “…high accumulation in various organs, such as the brain, is seen in sucklings when compared with adult animals. For example, the absorption rate (as % of oral dose) of 203Hg in one week- old suckling rats was 38.2%, whereas in 18-week-olds on either a milk diet or a standard diet, the rate was 6.7% and 1%, respectively.  The neurotoxicity of MeHg varies greatly between animal species. For example, nonhuman primates and cats metabolize MeHg similarly to humans, but rats and mice rapidly metabolize the compound to a less toxic inorganic form.” (12.4.5.3)

12.4.5.4            EFFECTS OF MERCURY ON HUMAN HEALTH

• “Coal-fired power plants are the largest source of anthropogenic Hg airborne emissions in the U.S. (40% of total emissions).” (12.4.5.4)

• “The critical organ concentration of MeHg may differ for different stages of the human life cycle.  The developing fetal and newborn brain may be the most sensitive organ (i.e., critical organ) in terms of human MeHg toxicity. … It was concluded that MeHg had crossed the placenta and that the fetal brain was much more sensitive than the adult brain. … In this outbreak, an infant’s blood Hg level was found to be higher than the mother’s during the first few months of life, supporting the suggestion that the fetal brain is the critical organ in the exposed pregnant female.” (12.4.5.4)

• “…Alkylorganic Hg is most likely to accumulate in nervous tissue.” (12.4.5.4)

• “Pronounced brain damage occurs in victims of Hg poisoning. The biological half-life of Hg is estimated to be 70 days. The critical daily intake has been estimated to be 300 mg Hg as MeHg for an average 70-kg man.  Chronic Hg poisoning may result from exposure to small amounts of Hg over long periods… The victim experiences extreme salivation and thirst, nausea, severe gastrointestinal irritation, and abdominal pain. [colic, anyone?] Loss of fluids and electrolytes occurs.” (12.4.5.4)

• “It was reported that she was apparently transferring dimethylmercury in a fume hood when 0.1 to 0.5 ml of the compound spilled on the disposable latex gloves she was wearing and permeated them, quickly seeping into her skin. She became ill a few months later and died of Hg poisoning less than a year after the exposure.” (12.4.5.4)

12.4.6               BIOLOGICAL EFFECTS OF MERCURY

• “Mercury, like many other heavy metals, is extremely toxic because as an ion or in certain compounds it is soluble in water. For this reason it is readily absorbed into the body, where it tends to combine with and inhibit the functioning of various enzymes. The ultimate effects of Hg in the body are similar to those of Pb and Cd: inhibition of enzyme activity and cell damage.” (12.4.6)

• “Inhibits the active transport mechanism, destroys mitochondrial apparatus, causes swelling of cells, leading to lysis, suggested liver dysfunction, decreases DNA content in cells and adversely affects chromosomes and mitosis, leading to mutagenesis…appears to be cytotoxic as it alters the rates of DNA, RNA, and collagen synthesis.” (12.4.6)

• “The MT protein receptor present in kidney tissue tends to bind actively with Hg and may thus exercise a protective effect. When the MT receptors are saturated with Hg, morphologic damage becomes manifest. An adaptive mechanism may also exit; MT content in the kidneys increases with repeated Hg exposure.” (12.4.6)

12.4.7               MERCURY AND NUTRITION

• “Dietary Se [Selenium] has been shown to exhibit a protective effect against Hg toxicity. Treatment with Se reduced the lethal and neurotoxic effects of MeHg and other Hg compounds. The reason for this protective action is not clear.” (12.4.7)

• “In addition to Se, vitamin E is also known to protect against the toxic effect of MeHg. However, a much higher concentration of this vitamin is required to provide the same level of protection.” (12.4.7)

• “Ascorbic acid added to the diet of chicks was shown to overcome growth depression caused by 500 ppm Hg. … High dietary levels of ascorbic acid might result in increased urinary excretion of cations to balance the excretion of the ascorbate anion and thus increase the rate of excretion of toxic elements.” (12.4.7)

ENVIRONMENTAL TOXICOLOGY – Second Edition
Biological and Health Effects of Pollutants
Ming-Ho Yu
ISBN: 1-56670-670-X

One of the most visible functions of the PR department is to help management plan for and respond to crisis. A good PR professional looks for potentil problems, constantly scans the business environment, then alerts management to the implications of such problems, and suggests the best course of action.

Disasters of earthquake proportions fall into the category of public relations nightmares created by sudden , violent accidents. Plane crashes, oil spills, chemical leaks, and product defects all belong to this group. The other type of crisis is the sort that builds slowly and occurs because of a company’s conscious, but ill-founded, decisions.

Whn disaster strikes , a defensive posture is generally counterproductive. The best course is to be proactive, admit your mistakes and apologize.

When disaster hits most companies respond, to some degree, through their public relations department, but they often ignore the audience that is likely to be hit hardest—employees. To minimize the impact of any crisis on employees, be sure to communicate honestly, openly, and often, actively encourage employees to share their concerns, and use caution when sharing personal opinions.

My Consultancy–Asif J. Mir - Management Consultant–transforms organizations where people have the freedom to be creative, a place that brings out the best in everybody–an open, fair place where people have a sense that what they do matters. For details please visit www.asifjmir.com, Lectures, Line of Sight

I recently saw a patient who had a complaint of having two ear canals in each of the ears. To my surprise, the patient had exactly that! You can see the second ear canal in the picture below… it is above the normal one and is about 25% the size.

To those in the know, this is due to a congenital birth defect related to the first branchial cleft.

Read more about this birth defect here. Clearly, the way to correct this is surgical.

Care aveti un Nokia 1100 puteti sa-l scoateti la vanzare. Ia uitati ce scrie aici.
Sau puteti sa-l tineti si sa-l folositi voi in scopuri malefice cum ar fi extragerea de multi bani din conturi, asta dac-ar mai exista banci care sa-ti transmita astfel de detalii prin sms.
Oricum, sa ma anuntati si pe mine daca a iesit ceva, ca tare imi mai plac povestile astea.

PS: Si eu care credeam ca doar romanii sunt mai creduli asa, de felul lor.

În urmă cu câteva zile am început să am nişte probleme destul de ciudate cu laptopul.
Totul a pornit de la un ecran care licărea ca la discotecă. Problema părea cât de cât a fi localizată, deşi nu era deloc îmbucurător faptul că laptopul se mai oprea din senin chiar dacă output-ul video era directat prin VGA către un monitor extern.

De aseară merge iar cum trebuie. Bănuiam că poate fi şi o problemă legată de supraîncălzire – placa video are de regulă ~70 C. Totuşi, nu cred că aspirarea ventilatorului sau montarea unor picioruşe de cauciuc mai înalte au vreo contribuţie decisivă. E foarte ciudat.

Căutând prin Event log, am găsit nişte erori care mă trimit deja pe o altă pistă: procesor-memorie-Windows 7(?).
Două evenimente se repetă destul de des, cam la fiecare pornire:

WHEA-Logger EventID 19 Warning
A corrected hardware error has occurred.

Reported by component: Processor Core
Error Source: Machine Check Exception
Error Type: Cache Hierarchy Error
Processor ID: 1

WHEA-Logger EventID 18 Error
A fatal hardware error has occurred.

Reported by component: Processor Core
Error Source: Machine Check Exception
Error Type: Bus/Interconnect Error
Processor ID: 1

(mesajele pe care le-am programat să apară ori de câte ori sunt detectate cele două erori; de fiecare dată când pornesc calculatorul privesc la acest memento mori)

Am mai găsit în puţine locuri pe net schimburi de mesaje legate de erorile astea (exemplu). De cele mai multe ori, la mijloc era un procesor AMD şi un sistem de operare Windows Vista sau 7. Nu ştiu dacă e suficient pentru o concluzie de tip “procesor AMD + Windows Vista/7 = bug”. E cam frustrant să ştii că problema există şi că poţi avea surpriza unei opriri din senin oricând, chiar când eşti în toiul lucrului la ceva important.

Am încercat să-l duc la reparat şi să contactez vânzătorul (emag). Până acum, niciun rezultat. Din câte pot observa, reparatul unui laptop nu-i deloc o treabă simplă, spre deosebire de cazul desktopurilor. Componentele se găsesc greu, atelierele de reparaţii sunt rare (ca de obicei, aproape toate se află în Bucureşti), timpul de reparaţie poate fi destul de mare, costurile, la fel.

Deja am luat în calcul foarte serios cumpărarea unui nou laptop. Nu-mi place deloc starea asta de incertitudine. Nu mă încântă nici ideea de a scoate din buzunar peste 20 de milioane. Nu este deloc momentul potrivit să cheltui mulţi bani.
De data asta, nu va mai fi un Acer şi nici nu va mai avea un procesor AMD. Cel mai probabil, nu-l voi mai cumpăra de la emag. M-am gândit la un Asus, cu procesor Intel Core2 Duo (exemplu). Asus nu este neapărat cea mai grozavă soluţie, însă e cel mai bun compromis între ceea ce vreau de la un laptop şi banii pe care aş fi dispus să-i plătesc.
Încă sunt în căutarea celui mai convenabil magazin: preţ cât mai mic, livrare la un cost decent, firmă de încredere (care să nu dea faliment în următorii doi ani, cât timp pot cere garanţia) şi, foarte important, service autorizat în România, cât mai aproape.

The European Union isn’t taking reports of potentially dangerous iPhone malfunctions lightly. EU Commissioner for Consumer Protection Meglena Kuneva issued a warning today that iPhones will be pulled from store shelves if it turns out recent screen explosions are hardware-based problems.

Kuneva says the issue is now in the hands of independent labs checking to see if it is in fact something integral to the devices that’s led to the incidents. Apple (s aapl) maintains that the problems are freak exceptions, and seems to have suggested to the EU Commission investigating the matter that users overheating lithium-ion batteries is what’s to blame.

For those not up to date, iPhone owners have reported several separate exploding screen incidents in a number of different countries, including EU member states. The similarity of the accounts and the behavior of the devices up to and including the actual explosions themselves, in addition to the mounting number of incidents reported, led the EU’s Commissioner for Consumer Protection to mount a full-scale investigation into the matter.

Apple’s line has always been that the problems are due to user abuse, not something wrong with the devices themselves. Claims by Commission members that Apple is specifically citing overheated lithium-ion batteries is the closest the company has come to pointing out a specific cause for the incidents.

Commissioner Kuneva also discussed what information she needs to act, and cited another case in which a product was proven dangerous and removed from market:

We need to have 100 percent certainty from one member state that these goods are dangerous. If I receive from the French authorities information that they are dangerous, I will act in the interests of the consumer. I will ask my network for a recall of the product as we did with the Italian (Senseo) coffee machines. There, it was proven that they burned the hands of consumers.

If confirmation comes from any member state investigating the matter in which one of the incidents occurred, a group which includes Britain and Germany in addition to France, the EU will stop the sale of the iPhone across all member countries. This won’t directly affect sales in other international markets, like the U.S., but other countries may be prompted to impose bans of their own following the EU’s findings.

There is little Apple can do at this point besides await the commission’s decision, since any admission of a hardware defect on its part would lead to a product recall and a cessation of sales anyway. Better to wait and see what independent lab testing shows, and have its hand forced in a worst-case scenario.