PARADE AT DYSNEYLAND,HONGKONG

MIND vs BRAIN

Most of us belive that  the brain is in charge, having evolved to control certain fixed behaviors. Why do men see other men as rivals for a desirable woman? Why do people seek God? Why does snacking in front of the TV become a habit? We are flooded with articles and books reinforcing the same assumption: The brain is using you, not the other way around. Yet it's clear that a faulty premise is leading to gross overreach.

The flaws in current reasoning can be summarized with devastating force:

1. Brain activity isn't the same as thinking, feeling, or seeing.

2. No one has remotely shown how molecules acquire the qualities of the mind.

3. It is impossible to construct a theory of the mind based on material objects that somehow became conscious.

4. When the brain lights up, its activity is like a radio lighting up when music is played. It is an obvious fallacy to say that the radio composed the music. What is being viewed is only a physical correlation, not a cause.

It's a massive struggle to get neuroscientists to see these flaws. They are king of the hill right now, and so long as new discoveries are being made every day, a sense of triumph pervades the field. "Of course" we will solve everything from depression to overeating, crime to religious fanaticism, by tinkering with neurons and the kinks thrown into normal, desirable brain activity. But that's like hearing a really bad performance of "Rhapsody in Blue" and trying to turn it into a good performance by kicking the radio.

We've become excited by a flawless 2008 article published by Donald D. Hoffman, professor of cognitive sciences at the University of California Irvine. It's called "Conscious Realism and the Mind-Body Problem," and its aim is to show, using logic, philosophy, and neuroscience, that we are not our brains. We are "conscious agents" -- Hoffman's term for minds that shape reality, including the reality of the brain. Hoffman is optimistic that the thorny problem of consciousness can be solved, and science can find a testable model for the mind. But future progress depends on researchers abandoning their current premise, that the brain is the mind. We urge you to read the article in its entirety, but for us, the good news is that Hoffman's ideas show that the tide may be turning.

It is degrading to human potential when the brain uses us instead of vice versa. There is no doubt that we can become trapped by faulty wiring in the brain -- this happens in depression, addictions, and phobias, for example. Neural circuits can seemingly take control, and there is much talk of "hard wiring" by which some activity is fixed and preset by nature, such as the fight-or-flight response. But what about people who break bad habits, kick their addictions, or overcome depression? It would be absurd to say that the brain, being stuck in faulty wiring, suddenly and spontaneously fixed the wiring. What actually happens, as anyone knows who has achieved success in these areas, is that the mind takes control. Mind shapes the brain, and when you make up your mind to do something, you return to the natural state of using your brain instead of the other way around.

It's very good news that you are not your brain, because when your mind finds its true power, the result is healing, inspiration, insight, self-awareness, discovery, curiosity, and quantum leaps in personal growth. The brain is totally incapable of such things. After all, if it is a hard-wired machine, there is no room for sudden leaps and renewed inspiration. The machine simply does what it does. A depressed brain can no more heal itself than a car can suddenly decide to fly. Right now the golden age of brain research is brilliantly decoding neural circuitry, and thanks to neuroplasticity, we know that the brain's neural pathways can be changed. The marvels of brain activity grow more astonishing every day. Yet in our astonishment it would be a grave mistake, and a disservice to our humanity, to forget that the real glory of human existence is the mind, not the brain that serves it.

WORLD TB DAY

World TB Day

Even singing can spread TB

1. Person–to–person transmission of TB occurs via inhalation of droplet nuclei (airborne particles 1 to 5 microns in diameter).
2. Coughing and singing facilitate formation of droplet nuclei.
3. Persons with active untreated respiratory tract disease (pulmonary or laryngeal) are contagious, particularly when cavitary disease is present or when the sputum is AFB smear–positive.
4. Patients with sputum smear–negative, culture–positive lung TB can transmit infection.
5. Extra pulmonary TB is not contagious unless the person also has lung TB.
6. Many procedures can result in the dispersal of droplet nuclei like endo–tracheal intubation, bronchoscopy, sputum induction, aerosol treatments, irrigation of a TB abscess, and autopsy.
7. Suspect TB if there is persistent (>3 weeks) cough and constitutional symptoms (fever, drenching night sweats, unintentional weight loss).
8. In HIV, the clinical and X–ray presentations of TB are often atypical. Such patients have an increased frequency of extrapulmonary TB and can have pulmonary disease despite a normal chest x–ray.
9. Results of acid–fast smears should be available within 24 hours.
10. Suspected or confirmed cases of TB should be reported promptly to the local public health department in order to expedite contact investigation and to help plan outpatient follow–up.
11. Suspicion of active pulmonary TB should prompt placement in an AII room. Such patients should be educated about the purpose of such isolation and instructed to cover their nose and mouth when coughing or sneezing, even when in the room. Whenever possible, procedures should be performed in the AII room to minimize exposure to the rest of the hospital. If the patient must leave the room, a surgical mask must be worn. All other persons entering the room must use respiratory protection, usually an N95 mask.
12. Anti–TB treatment administered during hospitalization should be directly observed therapy (DOT).
13. TB isolation rooms: Negative pressure is employed to prevent the escape of droplet nuclei. To accomplish this goal, doors must be kept closed and negative pressure should be verified daily. There must be 6–12 six air exchanges per hour. If recirculation to general ventilation is unavoidable, HEPA filters must be installed in the exhaust ducts.
14. Respiratory protection masks must filter particles 1 micron in diameter with at least 95% efficiency (N95) given flow rates up to 50 L per minute, must fit to a person’s face with less than 10% seal leakage. Health care workers should use these masks.
15. N 95 mask is designed to filter air before it is inhaled; thus, patients with known or suspected TB should not wear these masks. For the surgical masks are sufficient.
16. A patient may be transferred from an AII room once TB is ruled out or on treatment 3 consecutive sputum samples, obtained on different days, are smear–negative for AFB.
17. For patients with initially positive AFB smears, at least 2 weeks of TB treatment should be administered before isolation is discontinued.
18. For patients with MDR–TB, maintaining isolation throughout hospitalization is prudent.
19. Ideally a TB OPD clinic should be an AII room. If unavailable, an enclosed area should be used and a surgical mask (not an N95 mask) should be placed on the patient. The patient should be instructed to cover the mouth and nose with tissues when sneezing or coughing. If an area other than an AII room is used, it should not be used again for one hour once the patient has left.
20. An individual with AFB smear–positive involving the respiratory tract is generally considered to have been contagious starting three months before the first smear–positive sputum or onset of pertinent symptoms, whichever is earlier.
21. For persons with AFB smear–negative disease, the contagious period is considered to have begun one month before the onset of symptoms.
22. HCWs and patients with potential exposure should be screened (by symptoms and, unless positive at baseline, TST or IGRA) as soon as possible after the exposure. If initial screening is negative testing should be repeated 8 to 10 weeks following the end of the exposure.

URINARY TRACT INFECTION

Urinary tract infection is the most common bacterial infection encountered in the ambulatory care setting in the United States, accounting for 8.6 million visits in 2007. The self-reported annual incidence of urinary tract infection in women is 12%, and by the age of 32 years, half of all women report having had at least one urinary tract infection.

Clinical Pearls

• What are the risk factors for uncomplicated sporadic and recurrent cystitis and pyelonephritis?
Risk factors for uncomplicated sporadic and recurrent cases of cystitis and pyelonephritis include sexual intercourse, use of spermicides, previous urinary tract infection, a new sex partner (within the past year), and a history of urinary tract infection in a first-degree female relative. Case-control studies have shown no significant associations between recurrent urinary tract infection and precoital or postcoital voiding patterns, daily beverage consumption, frequency of urination, delayed voiding habits, wiping patterns, tampon use, douching, use of hot tubs, type of underwear, or body-mass index.
• Which organisms cause the majority of uncomplicated cystitis and pyelonephritis in women?
In women, E. coli causes 75 to 95% of episodes of uncomplicated cystitis and pyelonephritis; the remaining cases are caused by other Enterobacteriaceae, such as Klebsiella pneumoniae, and gram-positive bacteria such as Staphylococcus saprophyticus, Enterococcus faecalis, and Streptococcus agalactiae (group B streptococcus). However, the latter two organisms, when isolated from voided urine from women with uncomplicated cystitis, often represent contamination of the voided specimen.

Morning Report Questions

Q: What are the classic symptoms of cystitis versus pyelonephritis and how does one approach the diagnosis?
A: Cystitis is usually manifested as dysuria with or without frequency, urgency, suprapubic pain, or hematuria. Clinical manifestations suggestive of pyelonephritis include fever (temperature >38 degrees C), chills, flank pain, costovertebral-angle tenderness, and nausea or vomiting, with or without symptoms of cystitis. Dysuria is also common with urethritis or vaginitis, but cystitis is more likely when symptoms include frequency, urgency, or hematuria; when the onset of symptoms is sudden or severe; and when vaginal irritation and discharge are not present. The only finding on physical examination that increases the probability of urinary tract infection is costovertebral- ngle tenderness (indicating pyelonephritis). Results of a dipstick test for leukocyte esterase or nitrites provide little useful information when the history is strongly suggestive of urinary tract infection, since even negative results for both tests do not reliably rule out the infection in such cases. A urine culture is indicated in all women with suspected pyelonephritis but is not necessary for the diagnosis of cystitis. Studies have shown that the traditional criterion for a positive culture of voided urine (10(5) colony-forming units [CFUs] per milliliter) is insensitive for bladder infection, and 30 to 50% of women with cystitis have colony counts of 10(2) to 10(4) CFUs per milliliter in voided urine. Since most clinical laboratories do not quantify bacteria below a threshold of 10(4) CFUs per milliliter in voided urine specimens, a culture report of “no growth” or “less than 10,000 CFU” in a woman with urinary symptoms should be interpreted with caution.
Q: How should episodes of recurrent cystitis be treated?
A: Episodes of cystitis that occur at least 1 month after successful treatment of a urinary tract infection should be treated with a first-line short-course regimen. If the recurrence is within 6 months, one should consider a first-line drug other than the one that was used originally, especially if trimethoprim-sulfamethoxazole was used, because of the increased likelihood of resistance. The authors’ recommendations for first-line therapy include nitrofurantoin, trimethoprim-sulfamethoxazole, fosfomycin, and pivmecillinam. Urinary symptoms that persist or recur within a week or two of treatment for uncomplicated cystitis suggest infection with an antimicrobial-resistant strain or, rarely, relapse. In such women, a urine culture should be performed, and treatment initiated with a broader-spectrum antimicrobial agent, such as a fluoroquinolone.

FDA WARNING ON STATINS

Statins may cause drug-drug interactions for patients taking drugs to treat HIV/AIDS or hepatitis C. FDA singled out atorvastatin, rosuvastatin, and simvastatin for the new warnings and restated a warning about mixing lovastatin with HIV and HCV drugs.
The FDA said that protease inhibitors taken with atorvastatin, rosuvastatin, simvastatin, or lovastatin increase the concentration of statins in the blood, which increases the risk for muscle injuries, including risk for rhabdomyolysis, which can cause permanent damage to the kidneys.
Atorvastatin is contraindicated with tipranavir plus ritonavir, and telaprevir and should be used with caution — at the lowest effective dose — among patients taking lopinavir plus ritonavir.
For patients taking darunavir plus ritonavir, fosamprenavir, forsamprenavir plus ritonavir, or saquinavir plus ritonavir, the atorvastatin dose should be limited to 20 mg daily. In patients taking nelfinavir, daily atorvastatin should not exceed 40 mg.
Rosuvastatin should be limited to 10 mg daily in patients taking altazanavir with or without ritonavir or lopinavir plus ritonavir.
Simvastatin  is contraindicated in patients taking “HIV protease inhibitors, boceprevir or telaprevir.”