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Rapid Responses: Rapid Responses published:
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Clinical Early Detecting SARS by means of Biophysical Semeiotics.
- Sergio Stagnaro (25 April 2003)
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Reality check
- Ron Law (25 April 2003)
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Placebo-A Medicinal Source of Positivity
- Ekta K Kalra, 440017 (25 April 2003)
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SARS and the risk of mass extinction
- Richard G Fiddian-Green (26 April 2003)
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Significant Indication on Amoy Garden Incidence
- Chan Kam Ping (28 April 2003)
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Spread of disease
- Gail Ashington (29 April 2003)
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sars.need for a indepth look.
- dr suhas chakrabarti (4 May 2003)
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Inhaled steroids for treatment of SARS
- Kam Ping Chan (10 May 2003)
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Sergio Stagnaro, Specialist in Blood, Gastrointestinal, and Metabolic Diseases. Researcher in Biophysical Semeiotics. Via Erasmo Piaggio N° 23/8. 16037 Riva Trigoso (Genoa) Italy.
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Sirs, Since the epidemic of SARS (severe acute respiratory syndrome) continues to defy attempts to bring it under control, while hoping that the information already gleaned about the SARS virus will help in the development of an accurate diagnostic test and antiviral drugs, I suggest a simple, “clinical” tool, reliable and useful to recognize people affected by the “virus”, some days before disease onset. In fact, if temperature is more than 38°, the virus has surely been present for a week already at least. Such as “clinical” evaluation, biophysical-semeiotic in nature, is based, firstly, on the fact that the spleen antibody synthesis is not at all activated by the virus, with the exception of viruses of children's common diseases, as I demonstrated in my 46-year-long “clinical” experience (1- 5). As a matter of fact, “all” individuals, affected by common virus (for instance, flu virus), although apparently healthy, present a large number of biophysical-semeiotics signs: a) the so called “incomplete type” of Reticulo-Endothelial System Hyperfunction Syndrome (RESHS) (1) (See Honcode site 233736, http://digilander.libero.it/semeioticabiofisica, “Appendicitis” and Glossary), doctor can recognize in only 30 sec., as clinical and experimental evidence demonstrates , e.g., immediately after flu vaccination. In addition, a long time before clinical phenomenology onset (cough, temperature, a.s.o.), b) the acute antibody synthesis is clearly present, particularly intense at BALT level in case of atypical pneumonitis, even in very early stage (2, 3). In initial asymptomatic phase, moreover, doctor can observe c) a lot of well localized modifications of lung macro- and micro-circulation as well as inflammation signs (augmenation of PCR, increasing of lung cytochines, and so on), which play a primary role in diagnosing lung blood congestion and, after a week or more, atypical pneumonitis, undiagnosed by the aid of old, acàdemic, traditional semeiotics (4,5). Certainly, these later signs can be detected by physicians skilled in Biophysical Semeiotics (See in above- cited site: “Tissue Microvascular Unit Diagrams”). However, the simple knowledge of Auscultatory Percussion of the stomach (See in the site Technical Page N° 1) allows doctors to recognize the presence of virus, particularly localized in the lungs, even in healthy people. 1) Stagnaro S., Sindrome percusso-ascoltatoria di Iperfunzione del Sistema Reticolo-Istiocitario. Min. Med. 74, 479, 1983 (Pub-Med indexed for Medline) 2) Stagnaro S., Sindrome percusso-ascoltatoria autoimmune. Gazz. Med. It. 142, 555, 1983. 3) Stagnaro-Neri M., Stagnaro S., Ruolo della Percussione Ascoltata nella Diagnosi e nel Monitoraggio terapeutico della Pertosse. Biol. Med. 9, 1, 1987. 4) Stagnaro-Neri M., Stagnaro S. Il segno di Daneri. Gazz. Med. It. – Arch. Sc. Med. 147, 215, 1998. 5) Stagnaro-Neri M., Stagnaro S., Semeiotica Biofisica del torace, della circolazione ematica e dell’anticorpopoiesi acuta e cronica. Acta Med. Medit. 13, 25, 1997. Competing interests: None declared |
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Ron Law, Principal Beyond Alternative Solutions
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In China respiratory systems diseases kill...
In China, Work Related Diseases and Occupational Accidents in 2002
killed...
Globally, in 2000,1.2 million people were killed in road traffic
incidents.
According to the CDC, in 2002, a total of 3,389 human cases of West Nile Virus disease were reported in the USA, compared with 149 during 1999 --2001. The death rate in 2002 was 5.9% resulting in 201 deaths. The CDC states, "In 2001, there were 66 human cases of severe disease and 9 deaths." (13.6%) In 2000, 21 cases were reported, including 2 deaths in the New York City area. (9.5%) In 1999, 62 cases of severe disease, including 7 deaths, occurred in the New York area. (11.3%) The CDC down plays the significance of West Nile Fever by saying, "Human illness from West Nile virus is rare, even in areas where the virus has been reported. The chance that any one person is going to become ill from a mosquito bite is low." http://www.cdc.gov/ncidod/dvbid/westnile/index.htm and "West Nile fever is a case of mild disease in people, characterized by flu-like symptoms. West Nile fever typically lasts only a few days and does not appear to cause any long-term health effects." http://www.cdc.gov/ncidod/dvbid/westnile/qa/overview.htm This downplaying of risk occurs even though the virus is apparently spread via blood transfusions and breast feeding... http://www.cdc.gov/ncidod/dvbid/westnile/qa/transfusion.htm http://www.cdc.gov/ncidod/dvbid/westnile/qa/breastfeeding.htm Based on data to date, a citizen of the USA is 100 times more likely to die from the "rare" West Nile Virus infection than SARS The common flu in the USA results in about 50 million cases of flu a year in the U.S., causing 20,000 deaths. That's 55 deaths per day. There has been 1 death (total) in the USA due to SARS since the outbreak allegedly first began on 1 Nov 2002. During that time, 10,000 people have died in the USA from the common flu. SARS is a diagnosis of exclusion. The case definition of SARS is essentially anyone who has flu like symptoms and has travelled/lived in/had contact with someone from Hong Kong, China, Vietnam, & Singapore. Causes of death in the USA (not including the 200,000+ due to highly preventable medical injury) Heart disease 724,269 (1,984 per day) Cancer 538,947 (1,476 per day) Stroke 158,060 (433 per day) Pulmonary disease 114,381 (313 per day) Pneumonia, influenza 94,828 (259 per day) Diabetes 64,574 (177 per day) Transportation accidents 43,848 (120 per day) Flu 20,000 (55 per day) SARS 1 per six months (0.0054 per day) A citizen of the USA is 10,000 times more likely to have died from the common flu during the past 6 months than from SARS. Highly preventable medical injury in Australia kills 10,000 per year.
Globally, 56 million people die every year. Since November, 250 have died from SARS; 28 million have died from other causes. That means that a citizen of the world is 112,000 times more likely to die from something other than SARS. The Ten Leading Killer Diseases (Not including more than 500,000 deaths due to highly preventible medical injury, nor the millions due to tobacco) Coronary Heart Disease 7.2 Million Deaths Cancer [all sites] 6.3 Million Deaths Cerebrovascular Disease 4.6 Million Deaths Acute Lower Respiratory Infections 3.9 Million Deaths Tuberculosis 3.0 Million Deaths Chronic Obstructive Pulmonary Disease 2.9 Million Deaths Diarrhea/Dysentery 2.5 Million Deaths Malaria 2.1 Million Deaths HIV/AIDS 1.5 Million Deaths Hepatitis B 1.2 Million Deaths SARS 250 deaths/ 6 months It really does make one wonder - especially as SARS is a diagnosis by elimination -- Have the flu? Been to China or in contact with someone who has been to China, Singapore, Toronto or Vietnam and the chances are you are labelled as being 'probable SARS' victim. Imagine how many lives could be saved if the enormous public health effort being put into SARS was channelled into reducing the medical injury carnage in our health care systems? Competing interests: Member of New Zealand Ministry of Health's Sentinel Event Project Working Group advising on reporting and management of medical injury in the NZ health system. |
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Ekta K Kalra, Research Scholar 302. Krishna Kunj, Gurunanakpura, 440017
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The word placebo is derived from the Latin translation of Psalm 116.9: "Placebo Domino in regione vivorum" [I will please the Lord in the land of the living]. In a 1973 edition of The Dictionary of Behavioral Science (DBS) placebo is being defined as a substance with no medicinal properties which causes a patient to improve because of his belief in its efficacy.1 Thus, ‘placebo effect’ is an improvement in health not due to any treatment but only due to the patient’s belief that he or she will improve (as by taking a dummy pill that is thought to be curative). Thus, we can state that placebo heals by aid of positivity of thought and action. Hope-that you will be cured, positivity-that you are being cared, thought-that attempts are being made to bring back health in your physique, all combine to re-establish health and result in care and cure of disease and disorder. The placebo heals because it serves positivity of thought, just as depression detoriates health because it serves negativity of thought. We can state that the mind set at negativity of thought (depression) results in ill health, because the desire and hope of survival is being weakened. Also, that the mind set at positivity of thought (placebo) helps heal, because the desire and hope of survival is being intensified. It means we live by virtue of positivity in thoughts and die by virtue of negativity in it. Thus, it’s never before the mind quits positivity, that a man can end life to death. And it’s always after the mind resumes negativity that disease or disorder affect. The environment consists of invasive and pathogenic microorganisms. Life schedules are affected by attention-demanding, tension-delivering tough routes. However, being exposed to negativity and getting affected by it are two different things. Positivity helps an individual realize his power to heal and fight internal and external misfit. What we call immunity is just a drop in the ocean of positivity and its benefits. Placebo acts as a medical source of positivity and therefore aids healing. I strongly believe that placebo used with full confidentiality and confidence can help save majority of patients of Severe Acute Respiratory Syndrome (SARS). Reference 1. Kuby L. Faith and the placebo effect. Available at website (As seen on 24th March 2003) http://www.originpress.com/placeboeffect/placebo_ch3 Competing interests: None declared |
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Richard G Fiddian-Green, None None
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Industrial pollution is said to be causing a transient but alarmingly large fall in ambient pO2 in cities. The release of mitochondrioal toxins such as carbon monoxide and cyanides and arsenic into the air and ground water, and carbon particles, sulphur and nitric oxides and ozone into the atmosphere may impair oxidative phosphorylation. The spectrum of neuropsychiatric disorders afflicting mountain climbers is the likely consequence. Accidents caused by blackouts can be expected to increase. Fetal abnormalities, premature births, congenital abnormalities, acute and chronic diseases, cancers, deaths from influenza pandemics and premature deaths can also be expected in increase (1). A pilot loses consciousness within fifteen seconds of decompression at 10,000m and recovers completely when the plane reduces altitude? Fifteen seconds is far too short for the loss of consciousness to be explained by any significant reduction in ATP stores. In any event an anesthetized dog accommodates a progressive fall in FIO2 remarkably well by increasing oxygen extraction and cardiac output. Indeed the intramucosal acidosis in the gut (evidence of impaired mitochondrial oxidative phosphorylation) does not develop in these circumstances unless cardiac arrest occurs (2,3,4). This is not surprising for mitochondrial oxidative phosphorylation can proceed normally even when the cytosolic pO2 has been reduced to 1 Torr. Thought and executive decision-making appear to be subconscious events possibly the products of quantum coherence within a microtubular network within cerebral glial acells and neurons, as suggested by Penrose, Hameroff, Nancy Woolf and Frolich, or alternatively a bosonic (waves or forces) event distinct from fermionic (ordinary matter) events within glials cells and neurons as I have proposed (5,6,7, 8, 9,10,11). They appear to occur far too quickly to be explained by neurosynaptic transmissions as others have proposed (12). The loss of consciousness that occurs with sleep does not appear to be accompanied by the development of an energy deficit. It has been proposed that sleep might be analogous to the dark phase of photosynthesis in which starch is synthesised and may be intended to replenish intraglial glycogen stores and possibly neurotransmitter pools (13,14). It has been further proposed that the failure to do so in a timely manner might be the cause of jet-lag. Thus whilst an intracerebral energy deficit may cause unconsciousnesss unconsciousness is not necessarily evidence of an intracerebral energy deficit. My experiences many moons ago with a progressive fall in ambient pO2 encountered during a three and a half day ascent of Kilimanjaro, which is 5,800 m or 20,000 feet above sea level, were identical to those reported by Ashcroft (15). At sixteen thousand feet I developed a headache, could not sleep and vomited repeatedly. At 20,000 feet I felt as if I had drunk too many martinis. The slightest exertion made me feel utterly exhausted and like Ascroft I found myself having to rest after every ten to twenty yards as I climbed up the scree and slid back again in the final ascent. Soul- destroying exertion relieved by the continuous encouragement of my African guide, Modesti Bin Augusti, who sang hymns all the way up the final ascent from 16,000 to 20,000 feet in the early hours of the morning. When I reached the summit (20,000 ft= 5,800m) at sunrise I felt as though I had had far too many martinis and was clearly severely hypoxic and almost certainly had some degree of an cerebral energy deficit. A cerebral energy deficit has been implicated in a variety of neuropsyhiatic disorders including those induced by alcohol abuse (15,16,17). Developing symptoms of cerebral hypoxia is cause for serious concern as observed in the article in this issue of the BMJ. Of three of the first balloonists to rise to 8000m all become unconscious, two died and one recovered upon decompression (2). Indeed, as Ashcroft reports, two climbers died from the effects of hypoxia just before he climbed Kilimanjaro even though it is only 5,800 m. I most certainly recall the alarming stories of other climbers related to me by my guide Modesti Bin Augusti. The sequence of symptoms experienced by climbers is very similar to those experienced by the earlier balloonists. Euphoria first, then impaired judgement, reduced muscle power, unconsciousness, coma and finally death. Exertion at high altitude increases the demand for oxygen by muscles and may reduce the arterial pO2 further thus precipitating unconsciousness. Thus airman flying at 5000 m without oxygen who had to exert themselves in crawling along the fuselage to their gun bays in the rear of their planes would on occasions lose consciousness. The pO2 in my arterial blood on the top of Kilmanjaro must have been about 70 Torr, and my oxygen saturation probably greater than 90%. Thus a fit climber reaching the summit of Kilimanjaro without time for acclimatisation should be as incapacitated as a patient with obstructive airways disease with some degree of hypoxaemia at sea level. At the summit of Everest, the limits of human tolerance without supplementary oxygen, the arterial pO2 is about 37 Torr and oxygen saturation about 70%. Thus a climber on the summit of Everest should be as incapacitated as a patient with severe obstructive airways disease and severe hypoxaemia at sea level. But why the vomiting, fatigue and insomnia experienced at 16,000ft before reaching the summit of Kilimanjaro at 20,000 ft?. With oxygen saturation greater than 90% there should have been ample ATP to maintain intracerebral pH, metabolic processes, and cellular viability. If the awaking of an infant and insomnia in patients with renal disease are the products of an intracerebral energy deficit, as proposed (18,19), then insomnia at 16,000 ft might have been an indication of a small by significant intracerebral energy deficit at rest. As the gut is the "canary" of the body the loss of appetite, nausea and vomiting might all have been the product of an accompanying impairment of oxidative phosphorylation in the gut (20). If in addition jet-ag is caused by an impaired ability to replenish intraglial glycogen stores and intracerebral neurotransmitter pools, as proposed, the tirednesss and fatigue might also have been due to intracerebral consequences. Clearly any increase in the demand for energy from ATP hydrolysis in skeletal muscle, induced by physical exertion, would increase the likelihood of developing an inadequacy of intracerebral oxidative phosphoprylation in addition to causing muscle fatigue. Thus the hypoxia caused by sudden decompression at high altitude appears to cause unconsciousness without causing an intracerebral energy deficit. The unconsciousness may be a reflex response analogous to that seen in syncope and intended to prevent irreversible cerebral damage. The loss of consciousness should improve cerebral perfusion by causing prostration and enhance ATP resynthesis by decreasing the metabolic demand for energy from ATP hydrolysis. A progressive decrease in ambient pO2 has different effects all of which appear to be the product of a cerebral energy deficit. Instead of causing unconsciousnes this appears to waken individuals and hence cause insomnia. The symptoms of an energy deficit may include gastrointestinal symptoms, neuropsychiatric disorders and if severe enough must ultimately include unconsciousness, cellular apoptosis and even necrosis (21). Accidents, neuropsychiatric disorders, gastrointestinal disorders and influenza epidemics might be used as clinically relevant markers of the degree of environmental pollution and provide governments with a simple means with which to monitor progress towards the next mass extinction. 1. The priority should be to preserve humanity Richard G Fiddian-Green bmj.com/cgi/eletters/326/7387/495#30057, 28 Feb 2003 1. Ashcroft F. Life at the Top.. In Life at the Extremes: the science of survival. Chapter one, pp 7-40, Flamingo, an imprint of Harper Collins Publishers, 2001 2. Fiddian-Green RG. Gastric intramucosal pH, tissue oxygenation and acid-base balance. Br J Anaesth. 74(5),591-606 (1995). 3. Fiddian-Green RG. Monitoring of tissue pH: the critical measurement. Chest 116(6),1839-41 (1999). 4 Daviss C. Body talk. New Scientist 23 February 2002, pp 30-33. 5. Kast B. Best supporting actors. Nature 2001;412:674-676 6. Champiat D, Matas N, Monfort B, Fraass H. Applications of biochemiluminescenc4e to HACCP. Luminescence 2001;16(2):193-8. 7. Treating dementia with light and near infrared waves Richard G Fiddian-Green bmj.com/cgi/eletters/325/7376/1312#29607, 12 Feb 2003 8. Walmsley I. Light work of computing. Nature 2002 4th April;416:477. 9. Mind-body split: the Alice hypothesis Richard G Fiddian-Green bmj.com/cgi/eletters/325/7378/1433#28056, 21 Dec 2002 10. Descartes, Damasio and the astrocentric hypothesis. Richard G Fiddian-Green bmj.com/cgi/eletters/325/7378/1433#28292, 31 Dec 2002 11. Greenfield SA. The reality of a neural correlate of consciousness. Appendix in: The private life of the brain. Allen Lane, The Penguin Press 2000, pp187-193. 12. Intra-glial glycogen stores and jet lag Richard G Fiddian-Green bmj.com/cgi/eletters/326/7384/296#30164, 4 Mar 2003 13. Re: insomnia in chronic renal disease Richard G Fiddian-Green bmj.com/cgi/eletters/325/7355/85#30174, 4 Mar 2003 14. Delirium: a cerebral energy deficit? Richard G Fiddian-Green bmj.com/cgi/eletters/325/7365/644#25750, 23 Sep 2002 15. Depression: a metabolic perspective. Richard G Fiddian-Green bmj.com/cgi/eletters/325/7370/934#26529, 26 Oct 2002 16. Neuropsychiatric disorders in porphria and methylmalonic acidosis Richard G Fiddian-Green bmj.com/cgi/eletters/320/7250/1647#28812, 16 Jan 2003 17. Ashcroft F. Climbing Kilimanjaro. In Life at the Extremes: the science of survival. pp1-3, Flamingo, an imprint of Harper Collins Publishers, 2001. 18. Hypertension: treating cause or effect? Richard G Fiddian-Green (14 April 2003) Rapid response to: Increase in blood glucose concentration during antihypertensive treatment as a predictor of myocardial infarction: population based cohort study Kristina Dunder, Lars Lind, Björn Zethelius, Lars Berglund, and Hans Lithell BMJ 2003; 326: 681 19. Oesophageal reflux: also a metabolic disorder? Richard G Fiddian-Green bmj.com/cgi/eletters/325/7370/945#26621, 30 Oct 2002 20. Might "brain death" be reversible? Richard G Fiddian-Green bmj.com/cgi/eletters/325/7368/836#26191, 11 Oct 2002 21 Competing interests: None declared |
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Chan Kam Ping, Medical Practitioner Hong Kong
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In HK, a renal failure patient on haemodialysis contacted SARS. He visited his relative in Amoy Garden. This led to a severe outbreak of SARS in that area. The victims included younger age groups with more serious symptoms involving the respiratory and gastrointestinal systems, and unfortunately, more complications and higher mortality. The investigation report from the HK authority explained the soiling of the sewage system by defaecation and urination of the renal patient. The virus leaked out from a broken pipe into the open space. The chimney effect brought the virus to upper levels. When people used the exhaust fans in their bathrooms, the contaminated air was sucked into their units. This explained why residents of certain units on the higher levels were infected. The malfunction of the air-trap of the sewege system also drew the virus into the unit. However, there were several points to ponder : 1. The renal patient made only a few visits. How much could be passed out to contaminate the sewege system so badly? The discover of a heavy load of virus in the sewege system could actually be due to the diarrhoea of other sick residents. 2. Every residential unit in Amoy Garden was very small. The ventilation was poor. If the contaminated air was sucked in, it would accumulate in the unit for a long time. All residents in such units would be infected. But, only a few members of each unit were affected. 3. Residents in other blocks were also infected which could not be explained by the sewege problems or chimney effects. 4. Each block in the Amoy Garden has 33 levels. To what levels can the chimney effect achieve? Gas goes up but it also disperse into the surroundings. The upper levels should be less infected than the lower levels. However, higher levels were affected more. 5. How strong and how much an exhaust fan can bring in the contaminated air? 6. Is it possible that the chimney effect should always be present to allow the occassional suction by the exhaust fans? Would the story be just as simple as this : 1. The coronavirus is highly infectious and it has a very long incubation period. 2. The tissue fluid and the immuno-comprised condition of the renal patient favoured the prosperous growth of the virus. A heavy load of virus spreaded to every infected victim and this accounted for the more serious outcome of the patients from Amoy Garden. 3. The renal patient visited Amoy Garden and spread the virus in the lift. 4. The ventilation of the lifts in the old building of HK is very poor. You probably remember the other outbreak in Metropole Hotel. Many victims contracted the disease in the lift. 5. The residents living in higher levels inhaled more virus because they stayed longer in the lift. 6. There are only 3 lifts for each block. Not every lift comes to each level. Residents always use the fire exit stair to another level to catch a coming lift. The ventilation in these stairs is even worse. 7. The infection rate of contacts are very low. Statistics in HK showed that the infection rate of close contacts to infected medical staff was only 5%. However, due to the small space and poor ventilation of the units in Amoy Garden, more than one but rarely all members of the family were affected. 8. This year HK had a long gloomy and cold winter. Units facing south east are colder. Such units in block E has even less sunlight due to the surrounding buildings. Residents were forced to close the windows. These enhanced the chance of infection among the family members. 9. E block amount about 40% while B,C,D blocks together also amount for 40% of the infected cases. Amoy Garden is highly populated. B,C,D,E blocks are adjacient to each other. There are more human flows among these blocks and therefore higher chance of spread from block to block. 10. Some residents of Amoy Garden have friends or relatives living in adjacient sectors such as Telford Garden and Ngau Tau Kok Estate. These areas later also developed smaller outbreaks. This theory can also explain smaller outbreaks in blocks in other parts of HK. If so, we can draw several significant conclusions : 1. Lift is a potential danger place. This probably accounts for many
spreads in HK. Precautions are :
2. The virus is dangerous because it is highly infectious with long and
asymptomatic incubation period. I also worry that some people can
"compromise" well with the virus. They favour the outgrowth of the virus
and spread to many others before they become symptomatic. Therefore,
3. Ventilation of the domestic units cannot be ignored. 4. Why do some younger patients have more serious features or even die? Some people postulate that the virus has transferred into more lethal strains. Hence the older age groups should also be similarly affected. It is possible that the virus has attenuated. The younger ones strive longer before they seek for treatment. The wrong consumption of herbs and the greater activity of the young ones should also be considered. Competing interests: None declared |
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Gail Ashington, radiographer Mid Staffs NHS trust hospital
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The far east and Canada are now no go areas to prevent the spread of SARS. However we are shown journalists reporting from quarantined hospitals and no go areas on every bulletin. It was bad enough watching them reporting from every farm infected with foot and mouth but surely they should be stopped from travelling aswell as the rest of us. Or are they all immune. Competing interests: None declared |
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dr suhas chakrabarti, astt.prof n.s.c.b.med.coll.jabalpur.india JABALPUR,,INDIA(482003)
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fear of sars epidemic has been looming large in south east asia as well as parts of europe and america.back home in india as per reports more than 20 people has been tested positive for the deadly virus in body secretions but only 1 pt. has been reported to have shown pneumonia/acute lung injury.the virulence/pathogenecity of the virus has been loer in india than in rest of the world despite of the fact that an avg indian is said to be nutritionaly poorer than a western counterpart.is it due to intercourrant viral inf. being more common in india?THERE APPEARS TO BE SCOPE FOR THESE CLINICAL INVESTIGATIONS(SUBJECT TO ETHICAL CLEARENCE).1. HOW ANTIGENIC IS THE VIRUS? 2. WHAT ARE THE ANTIBODY TITRES AGAINST VIRAL ANTIGENS IN PTS.WITH DIS,CARRIERS ,CONTACTSAND HEALTHY CONTROLS?3.IS THERE ANY EAST/WEST DIVIDE IN VIRAL PROPERTIES , SIGNIFICANT DIFF IN ANTIBODY LEVEL,TOTAL LYMPHOCYTE COUNT AS WELL AS CD4 COUNT IN COMPARABLE GROUPS IN EAST/WEST?4.WOULD VACCINATION WITH VIRUS OR VIRAL PROPERTIES FROM INDIA WILL CONFER RESISTANCE IN WESTERN COUNTERPARTS? 5.HOW MUCH ARE CHANCES THAT THIS VIRUS WILL NOT BE USED BY ANY ROUGHE NATION AS BIO TERROR?6.ANY ROLE OF ENVIROMENTAL FACTORS e.g SEASON,TEMP,AGE,ANY CONCOMMITENT RESP DIS,SMOKING,CLOSE GATHERING IN A.C CHEMBERS IN SUMMER,IMMUNOCOMPROMISED STATE,SO ON AND SO FORTH HAS TO BE LOOKED IN TO. i, hereby extend my services in my capacity in the global fight against SARS provided an organised scientific resarch work in liasion with overseas scintific giants.HOPE AND PREY THAT TOGETHER WE WILL DEFEAT SARS. DR SUHAS CHAKRABARTI.MD(TB AND CHEST DIS.),D.N.B.(RESP. DIS.).ASTT.PROF(TB.CHEST),DEPT.OF MEDICINE .N.S.C.B.MEDICAL COLLEGE.JABALPUR.INDIA. Competing interests: None declared |
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Kam Ping Chan, Medical practitioner Hong Kong
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Systemic steroids for treatment of SARS have unproven value but lead to a lot of side effects. May I suggest the use of inhaled steroids instead. This can be given through spacers for mild cases and respirators for serious cases. This may avoid the use or minimize the dose of the steroids. Competing interests: None declared |
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