Tuesday, July 29, 2008

anorexia

Many people with serious eating disorders seek mental-health care only after they are pressured into it by concerned clinicians, family, friends, and employers। Although these cases make psychiatrists uncomfortable, a new study suggests that coercion plays a valuable role in jump-starting participation in the treatment of eating disorders. http://louis2j2sheehan2esquire.blogspot.com

A team of psychiatrists studied people with eating disorders who had denied a need for treatment when they were admitted to a hospital clinic. Nearly half changed their minds and acknowledged the necessity of treatment within 2 weeks of being hospitalized, reports Angela S. Guarda of Johns Hopkins Hospital in Baltimore.

The predominantly female patients included many with anorexia nervosa and bulimia nervosa. In the former disorder, a person typically loses weight through starvation and exercise. People with bulimia alternate food-eating binges with induced vomiting.

The new study, published in the January American Journal of Psychiatry, focused on 139 patients admitted to a Johns Hopkins treatment program for eating disorders between January 2000 and February 2003. Patients ranged in age from 15 to 35. The program concentrates on establishing proper eating habits, restoring weight, and developing healthy attitudes toward food and personal appearance.

Each patient completed a 13-item questionnaire upon entering the program and again after 2 weeks of treatment। The questionnaire asked patients whether they needed hospitalization, whether they were coerced to join the program, and what their perceptions were of the hospital-admission process।http://louis2j2sheehan2esquire.blogspot.com

Of the 139 patients, 46 said at first that they were being coerced and didn't need hospitalization। Of that number, 20 switched after 2 weeks of treatment to saying that hospitalization had been justified। http://louis2j2sheehan2esquire.blogspot.com

The participants who changed their minds consisted of 14 of 34 anorexia patients and 6 of 12 bulimia patients.

Anorexia patients, who are often grossly underweight, reported more perceived coercion and less satisfaction with the admissions process than the bulimia patients did.

Guarda suspects that as these patients are tracked for longer periods during and after hospitalization, even more of them will switch to endorsing the treatment. The Johns Hopkins program lasts an average of 6 weeks.

Although the participants weren't legally bound to stay in the treatment program, none left during the first 2 weeks. Among those who had felt coerced, their willingness to stay "illustrates the ambivalence towards treatment that characterizes eating disorders," Guarda says.

"Many patients with anorexia nervosa remain untreated because no one pressured them into seeking treatment, and a significant proportion of them die," Guarda says. "The rest often lead isolated and very impaired lives."

It's compassionate to coerce individuals with eating disorders into treatment aimed at altering their potentially fatal pursuit of weight loss and thinness, comments psychiatrist Arnold E. Andersen of the University of Iowa Hospitals and Clinics in Iowa City.

Sunday, July 20, 2008

hyde

When the nefarious Mr. Hyde takes his own life, the good Dr. Jekyll is also killed.

Scientists are adopting the reverse approach for halting the protein behind prion diseases such as Creutzfeldt-Jakob and mad cow। By targeting the harmless version of the brain protein whose evil alter ego brings on disease, researchers have prevented the bad version of the protein from continuing its rampage in the brains of infected mice। The results are reported online July 14 in Proceedings of the National Academy of Sciences। http://louiskjksheehan।blogspot।comhttp://louiskjksheehan.blogspot.com

The approach of killing Jekyll to get Hyde is very promising, comments biochemist Sina Ghaemmaghami of the Institute for Neurodegenerative Diseases at the University of California, San Francisco। The sinister version of the protein comes in several slightly different forms, making it hard to develop a single attack strategy, Ghaemmaghami says। http://louiskjksheehan.blogspot.com

Led by neuroscientist Giovanna Mallucci of University College London, researchers delivered bits of attack RNA to interfere with production of the normal version of the prion protein. In animals who have prion disease, this protein somehow gets converted into a dangerous form, which then travels through the brain, coaxing other good versions of the protein to go bad.

The bad versions of the protein then clump together, a process that damages cells, although scientists aren’t exactly sure how.

“No one knows what the toxic entity is — that’s the black box,” says Mallucci.

It’s also a mystery how prions replicate — they seem to do it without DNA — and they are difficult to kill.

Using bits of RNA that interfere with protein production has potential as a therapy for treating many neurodegenerative diseases, but those therapies are a ways off, says Ghaemmaghami. In the new study, researchers injected the interfering RNA, packed in a lentivirus, into the hippocampus of rodents already given a diseased version of the protein. Treated animals lived longer and had fewer symptoms of prion disease.

But getting therapeutic molecules into the human brain is another story, especially molecules as big as RNA. “The brain is just about the hardest place to get into,” Ghaemmaghami says.

In a separate study, researchers have come closer to understanding what PrP, the innocuous Dr. Jekyll version of the prion protein, does for a living. The PrP protein is found in most brain cells, but its function remains a mystery. Mice engineered to not have the PrP protein appear relatively healthy. The slight differences scientists have noted is that PrP-free mice don’t perform quite as well as their normal counterparts on some learning and memory tasks and also don’t recover as well from seizures or strokes.

To investigate the role of regular PrP, Gerald Zamponi and colleagues at the University of Calgary in Canada looked at communication among the brain cells of PrP-free mice. When the nerve cells received the messenger molecule known as glutamate, they went into hyperactive mode, repeatedly firing as if the message had been shouted at them, says Zamponi. These overexcited cells were more likely to die because of this overactivation, the scientists report in a recent Journal of Cell Biology.

Normal PrP protein might function to block some NMDA receptors and thereby prevent overexcitement of certain neurons, says Zamponi.

The researchers also removed magnesium from the cells. Magnesium usually blocks some of the receptors that catch the NMDA messages. Without it, the brain cells went into seizure mode, further evidence that the PRP-free mice were super-sensitive to NMDA.

The PrP protein seems to have emerged late in vertebrate evolution—there is no version that scientists can scrutinize in critters like yeast and fruit flies. While it is too early to conclusively identify its role, investigating what the good version of the protein does has merit, says UCSF’s Ghaemmaghami.

After all, that’s how the good Dr. Jekyll’s friends learned the origin of the deadly Mr. Hyde.

Wednesday, July 9, 2008

breezes

Fair and warm, with pleasant breezes.

Gen. Johnston, without a defeat, has fallen back to Calhoun, Ga. Gen. Lee, without a defeat, has fallen back to Hanover Junction, his headquarters at Ashland. http://louis0j0sheehan0esquire.blogspot.comGrant is said to be worming his way eastward to the Peninsula, the field occupied by McClellan in 1862। Why, he might have attained that position without the loss of a man at the outset! http://louis0j0sheehan0esquire.blogspot.com

On Saturday night Gen. Butler made the following exploit:

“On Saturday night the enemy renewed his assault, assailing that portion of our line held principally by Wise’s brigade. In some manner our men had become apprised of the intention of the enemy to make a night attack, and were fully prepared for it. The enemy were allowed to advance, our men deliberately reserving their fire until they were within 20 or 30 yards of them, when they poured into their ranks a most terrific volley, driving them back with great slaughter. The repulse is said to have been a most decided success; the enemy were thrown into great confusion and retreated rapidly.

“The enemy’s loss is said to have been very severe, and is estimated at hardly less than four or five hundred in killed alone, while we are said to have lost none in killed, and some thirty or forty wounded.”

There was an immense mail to-day, and yet with my sore eyes I had no aid from my son, still at the intrenchments. I hinted my desire to have him, but young Mr. Kean opposed it.

Saturday, June 28, 2008

information

An approach loosely based on Information theory uses a brain-as-computer model। In adaptive systems, a system may use feedback to increase the signal-to-noise ratio, which may converge towards a steady state. http://Louis2J2Sheehan2Esquire.USIncreasing the signal-to-noise ratio enables messages to be more clearly received from a source. The hypnotist's object is to use techniques to reduce the interference and increase the receptability of specific messages (suggestions). http://Louis2J2Sheehan2Esquire.US

Systems theory, in this context, may be regarded as an extension of James Braid's original conceptualization of ह्य्प्नोसिस as involving a process of enhancing or depressing the activity of the nervous system. Systems theory considers the nervous system's organization into interacting subsystems. Hypnotic phenomena thus involve not only increased or decreased activity of particular subsystems, but also their interaction. A central phenomenon in this regard is that of feedback loops, familiar to systems theory, which suggest a mechanism for creating the more extreme hypnotic phenomena.

Thursday, June 19, 2008

resolution

IKONOS comes from the Greek word for "image". Ikonos-1 was planned for launch in 1999 but the launch failed. Ikonos-2 was planned for launch in 2000, but was renamed Ikonos and was launched on September 24, 1999 from Space Launch Complex 6 (SLC-6) at Vandenberg Air Force Base in California to replace Ikonos-1. The imaging sensors are panchromatic and multispectral. This satellite has a polar, circular, sun-synchronous 681-km orbit and both sensors have a swath width of 11 km. Its weight is 1600 pounds (720 kg). Space Imaging was acquired by ORBIMAGE to form GeoEye.

[edit] Specifications http://Louis-J-Sheehan.de

[edit] Spacecraft

Ikonos-2 is a 3-axis stabilized spacecraft, using the LM900 satellite bus system (also referred to as Block-1). The attitude is measured by two star trackers and a sun sensor and controlled by four reaction wheels; location knowledge is provided by a GPS receiver. The design life is 7 years; S/C body size=1.83 m x 1.57 m (hexagonal configuration); S/C mass = 817 kg; power = 1.5 kW provided by 3 solar panels.

The LM900 spacecraft is a three-axis stabilized bus that is designed to carry scientific payloads in LEO orbits. It provides precision pointing on an ultra stable highly agile platform. Payloads for a variety of scientific and remote sensing applications may be accommodated including laser sensors, imagers, radar sensors, electro-optical and astronomical sensors, as well as planetary sensors. The LM900 spacecraft design was based on the CRSS imaging bus. Hardware heritage is from CRSS and IRIDIUM.
http://Louis-J-Sheehan.de
[edit] Communications

IKONOS conducts telemetry, tracking and control in the 8345.968-8346.032 MHz band (downlink) and 2025-2110 MHz band (uplink). Downlink data carrier operates in the 8025-8345 MHz band.

[edit] Spatial resolution

* 0.8 m panchromatic (1-m PAN)
* 4-meter multispectral (4-m MS)
* 1-meter pan-sharpened (1-m PS)

Spectral Resolution
Band 1-m PAN 4-m MS & 1-m PS
1 (Blue) 0.45-0.90 µm 0.445-0.516 µm
2 (Green) * 0.506-0.595 µm
3 (Red) * 0.632-0.698 µm
4 (Near IR) * 0.757-0.853 µm

[edit] Temporal resolution

The revisit rate for IKONOS is 3 to 5 days off-nadir and 144 days for true-nadir.

[edit]

Thursday, June 12, 2008

napoleon Louis J. Sheehan, Esquire 22311

A hair trail has now shed light on a two-centuries-old historical question.

Napoleon Bonaparte, the famous dictator of France, died in exile on the island of St. Helena in the southern Atlantic Ocean. While doctors at the time cited stomach cancer as the cause of death, some historians believe that arsenic did him in—high levels of the toxic substance were found in hair samples after he died. But not so fast, says a team of Italian scientists—the arsenic in Napoleon’s hair probably didn’t kill him.

The scientists took samples of Napoleon’s hair from the collections of museums in Rome, Paris, and Parma, Italy, which date from his boyhood, his first exile on Elba in 1814 and his death in 1821 . Upon putting the hairs into a nuclear reactor—radiation allows scientists to identify the elements present, and apparently doesn’t bother the hairs—the researchers found that Napoleon had consistent arsenic levels in his body his whole life, not just one spike in the end that doomed him. The levels are very high, but that makes sense—small doses of arsenic were used as a health tonic in Napoleon’s day, and medicines with tiny arsenic concentrations are still used today.

Hairs aren’t the only historical artifacts that have been brought into the Napoleon death foray. In 2005, scientists studied his pants, and found that the little corporal was even littler at his death, having dropped almost 5 inches on his waist, which the Swiss researchers said parallels the weight drop of modern stomach cancer patients.

So if the Italians are right, Napoleon’s original doctors have been vindicated. And they have his hair and trousers to thank.

Tuesday, June 3, 2008