Sunday, 28 August 2016

He asked the question??????? I will answer it.

David Attenborough wondered why a sea creature's shell was spiral, well every move we make, down to gravity is rotational, else we couldn't function.

Wednesday, 24 August 2016

English Doctors - "ms" and many other neurological diseases have been made up, Doctors and nurses have been trained WRONG

GPs in England say they lack confidence in initially assessing and referring people with neurological symptoms, especially those with multiple sclerosis, and believe they could benefit from better training in identifying and managing neurological patients.
According to a report published by the Neurological Alliance a majority of patients now wait more than a year between the time they begin noticing symptoms and the time they first see a specialist. Because most neurological conditions are progressive and early treatment is critical to reducing disease progression and severity, such delays in accessing secondary care can have strong consequences for the patients.
In this new report, researchers focused on the perspective of GPs regarding problems in the assessment and management of people with neurological signs and symptoms.
The team found that although the vast majority (94 per cent) of GPs are “somewhat confident” or “extremely confident” in assessing and referring potential diabetics, that confidence declines considerably for patients with neurological conditions. Only 81 per cent expressed confidence in making an initial assessment and referral for epilepsy, 73 per cent for Parkinson’s disease, and 47 per cent for multiple sclerosis.
In addition, 85 per cent of GPs in England were either “somewhat concerned” or “extremely concerned” about the time it took for a potential neurological patient to be examined by a neurologist. More than half (almost 60 per cent) also felt that local services and systems in their area were not sufficient for patients to receive a timely diagnosis.
A vast majority of GPs, 84 per cent, also felt they could benefit from further training in identifying and managing people with multiple sclerosis, Parkinson’s, or other neurological conditions.
The report includes nine recommendations to strengthen GP experience and confidence during initial visits from these patients. These include a call for the development of a pan-neurological “watch list,” identifying the 10 common signs and symptoms that GPs need be aware of during patient interactions in primary care settings, and a call to increase the number of local neurologists who receive referrals from primary care, as well as their capacity and resources.
“It is essential that NHS [National Health Service] England and the Department of Health respond to these findings and engage with the concerns of GPs and people living with neurological conditions,” Arlene Wilkie, CEO of the Neurological Alliance, said in a press release. “Without an effective pathway through primary care, patients will continue to suffer the consequences of undue delays to referral, diagnosis and treatment, and outcomes will continue to suffer.”
Source: Multiple Sclerosis News Today © Copyright 2014 - 2016 BioNews Services, LLC (23/08/16)

Tuesday, 23 August 2016

Selenium - I have just watched film Evolutionn


Selenium yeast

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Selenium yeast, produced by fermenting Saccharomyces cerevisiae in a selenium-rich media, is a recognized source of organic food-form selenium.[1] In this process, virtually all of the selenium structurally substitutes for sulfur in the amino acid methionine thus forming selenomethionine via the same pathways and enzymes that are used to form sulfur-containing methionine. Owing to its similarity to S-containing methionine, selenomethionine is taken up nonspecifically and becomes part of yeast protein. It is this metabolic route that makes selenium yeast valuable in animal and human nutrition, since it offers the same organic form of selenium produced by food-chain autotrophs (i.e., most plants and certain blue-green algae).[1][2]


Human health applications[edit]

Selenium is physiologically essential and may also offer a protective effect against several degenerative diseases.[3] The organic form of selenium provided by selenium yeast has been shown to differ in bioavailability and metabolism compared with inorganic (e.g., selenate, selenite) forms of dietary selenium.[4] Dietary supplementation using selenium yeast has been associated with increased ability to counteract oxidative stress.[5] Furthermore, selenium yeast has been used in a wide range of studies aimed at examining the importance of selenium status in the incidence and progression of a variety of infectious and degenerative diseases.[6]
  • Cancer. Although selenium is promoted for its claimed anti-cancer effect, there is no good evidence of it being helpful in treating or preventing cancer, or with helping alleviate the side-effects of cancer treatment.[7][8][needs update] Dietary supplementation with selenium yeast has been used to study the effects of selenium status and the risk of developing cancers or precancerous lesions.[9]
  • Viral infection. Findings of increased viral virulence in selenium-deficient hosts support the need for further investigation into the interaction between host nutrition and viral evolutionary processes.[10][11][12] Certain viral diseases have been shown to mutate more rapidly in selenium-deficient hosts producing more virulent viruses. This etiology has been demonstrated for both the Coxsackie B virus (associated with a Se-deficiency-related cardiomyopathy known as Keshan disease)[13] and the influenza virus.[14] High selenium yeast supplementation (200 μg/d) was evaluated in a 9-month double-blind, randomized, placebo-controlled trial in HIV-positive adult men and women. Daily supplementation was found to suppress progression of HIV-1 viral burden and provide indirect improvement to CD4 cell counts.[15] (Selenium status diminishes with HIV disease progression; low selenium status has been shown to be a predictor of HIV-related mortality.[16][17] Selenium deficiency has also been linked with increased infectiousness of people with HIV-1.[18] )

Animal feed and food-animal product applications[edit]

Selenium supplementation in yeast form has been shown to have beneficial effects in many species, especially on animal immune status,[19] growth[20] and reproduction[21][22][23][24][25] The consequent improvements in productivity can be of economic benefit to livestock producers for many reasons, including greater overall efficiency of feedstuff use.
Selenium yeast supplementation of food-animal diets has an added nutritional benefit to human consumers of food-animal products. Dietary selenomethionine-containing plant or yeast protein can be also stored nonspecifically in animal protein, which can result in nutritionally useful selenium content in meat, milk, and eggs. Consequently, strategies to supplement animal feed with selenium yeast have led to the development of selenium-rich functional foods, including selenium-enriched eggs and meats for human consumption.[26][27][28][29]

Safety[edit]

Since 2000, selenium yeast (S. cerevisiae CNCM I-3060) has been reviewed and received the following approvals for use in animal and human diets:
  • U.S. Food and Drug Administration (FDA) approval for use as a supplement to feed for chickens, turkeys, swine, goats, sheep, horses, dogs, bison, and beef and dairy.[30]
  • European Food Safety Authority (EFSA) approval for use as a feed supplement for all animal species and categories.[31]
  • Organic Materials Review Institute approval for use as a feed supplement for all animal species.[32]
  • European Food Safety Authority (EFSA) approval for human health claims linking dietary intake of selenium yeast to "protection of DNA, proteins and lipids from oxidative damage, normal function of the immune system, normal thyroid function and normal spermatogenesis."[33]
A review of the scientific literature concluded that selenium yeast from reputable manufacturers is adequately characterised, of reproducible quality, and shows no evidence of toxicity in long-term supplementation studies at doses as high as 400 and 800 micrograms per day (exceeding the EC tolerable upper intake level of 300 micrograms per day).[34]

Analytical chemistry[edit]

Total selenium in selenium yeast can be reliably determined using open acid digestion to extract selenium from the yeast matrix followed by flame atomic absorption spectrometry.[35] Determination of the selenium species selenomethionine can be achieved via proteolytic digestion of selenium yeast followed by high performance liquid chromatography (HPLC) with inductively coupled plasma mass spectrometry (ICP-MS).[36][37][38]

References[edit]

  1. ^ Jump up to: a b Schrauzer G (2006). "Selenium yeast: composition, quality, analysis, and safety". Pure Appl Chem. 78: 105–109. doi:10.1351/pac200678010105. 
  2. Jump up ^ Schrauzer GN (2003). "The nutritional significance, metabolism and toxicology of selenomethionine". Adv Food Nutr Res. 47: 73–112. doi:10.1016/s1043-4526(03)47002-2. 
  3. Jump up ^ Navaro-Alarcon M, Lopez-Martinez M (2000). "Essentiality of selenium in the human body: relationship with different diseases". Sci Tot Environ. 249: 347–371. doi:10.1016/s0048-9697(99)00526-4. 
  4. Jump up ^ Schrauzer G. Selenomethionine: A review of its nutritional significance, metabolism and toxicity" J Nutr 2000;130:1653-1656.
  5. Jump up ^ Ravn-Haren G, Bugel S, Krath B, et al. (2008). "A short-term intervention trial with selenate, selenium-enriched yeast and selenium-enriched milk: effects on oxidative defence regulation". Br J Nutr. 99: 883–892. doi:10.1017/s0007114507825153. 
  6. Jump up ^ Lovell M, Xiong S, Lyubartseva G, Markesbery W (2009). "(Sel-Plex diet) decreases amyloid burden and RNA and DNA oxidative damage in APP/PS1 mice". Free Radic. Biol. Med. 46: 1527–1533. doi:10.1016/j.freeradbiomed.2009.03.008. 
  7. Jump up ^ "Selenium". American Cancer Society. 7 March 2011. Retrieved June 2014.  Check date values in: |access-date= (help)
  8. Jump up ^ Dennert G, Zwahlen M, Brinkman M, Vinceti M, Zeegers MP, Horneber M (2011). "Selenium for preventing cancer". Cochrane Database Syst Rev (5): CD005195. doi:10.1002/14651858.CD005195.pub2. PMC 3692366free to read. PMID 21563143. 
  9. Jump up ^ Combs GJ, Lu J. Selenium as a cancer preventive agent. In: Hatfield D, Berry M, eds. Selenium: Its molecular biology and role in human health, 2nd ed. New York: Springer, 2006: 249-264.
  10. Jump up ^ Beck M. Selenium and viral infections. In: Hatfield D, Berry MJ, Gladyshev VN, eds. Selenium: Its molecular biology and role in human health, 2nd ed. New York: Springer, 2006: 287-298.
  11. Jump up ^ Beck M (2001). "Antioxidants and viral infections: Host immune response and viral pathogenicity". J Am Coll Nutr. 20: 384S–388S. doi:10.1080/07315724.2001.10719172. 
  12. Jump up ^ Beck M, Matthews C (2000). "Micronutrients and host resistance to viral infection". Proc Nutr Soc. 59: 581–585. doi:10.1017/s0029665100000823. 
  13. Jump up ^ Levander O, Beck M (1999). "Selenium and viral virulence". Br Med Bull. 55: 528–533. doi:10.1258/0007142991902592. 
  14. Jump up ^ Beck M, Nelson H, Shi Q, et al. (2001). "Selenium deficiency increases the pathology of an influenza virus infection". FASEB J. 15: 1481–1483. doi:10.1096/fj.00-0721fje. 
  15. Jump up ^ Hurwitz B, Klaus J, Llabre M, et al. (2007). "Suppression of human immunodeficiency virus type 1 viral load with selenium supplementation". Arch Intern Med. 167: 146–154. doi:10.1001/archinte.167.2.148. 
  16. Jump up ^ Baum M, Shor-Posner G, Lai S, et al. (1997). "High risk of HIV-related mortality is associated with selenium deficiency". JAIDS. 15: 370–374. doi:10.1097/00042560-199708150-00007. 
  17. Jump up ^ Baum M, Camps A. Role of selenium in HIV/AIDS. In: Hatfield D, Berry MJ, Gladyshev V, eds. Selenium: Its molecular biology and role in human health, 2nd ed. New York: Springer, 2006: 299-310.
  18. Jump up ^ Baeten J, Mostad S, Hughes M, et al. (2001). "Selenium deficiency is associated with shedding of HIV-1-infected cells in the female genital tract". JAIDS. 26: 360–364. doi:10.1097/00126334-200104010-00013. 
  19. Jump up ^ Sarkuniene C, Oberauskas V, Baranauskiene D, et al. (2010). "The impact of forage additive Sel-Plex containing organic selenium (Se) on morphological and biochemical blood parameters and activity enzymes GPx and δ-ALRD in fattening pigs". Vet Med Zoot. 50: 88–92. 
  20. Jump up ^ Pappas A, Acamovic T, Surai PF, McDevitt R. Maternal organo-selenium compounds and polyunsaturated fatty acids affect progeny performance and levels of selenium and docosahexaenoic acid in the chick tissues. Poult Sci 2006;85:1610-1620.
  21. Jump up ^ Dimitrov S, Atanasov V, Surai PF, Denev S (2007). "Effect of organic selenium on turkey semen quality during liquid storage". Anim Reprod Sci. 100: 311–317. doi:10.1016/j.anireprosci.2006.07.007. 
  22. Jump up ^ Slowinska M, Jankowski J, Dietrich G, et al. (2011). "Effect of organic and inorganic forms of selenium in diets on turkey semen quality". Poult Sci. 90: 181–190. doi:10.3382/ps.2010-00956. 
  23. Jump up ^ Ebeid T (2009). "Organic selenium enhances the antioxidative status and quality of cockerel semen under high ambient temperature". Br Poult Sci. 50: 641–647. doi:10.1080/00071660903303415. 
  24. Jump up ^ Zhao L, Xu S, Zhao R, Peng Z, Pan X. "Effects of selenium and methionine supplementation of breeder hen diets on selenium concentration and oxidative stability of lipids in the thigh muscles of progeny. J Food Sci 2009;74:C569-AC574.
  25. Jump up ^ Thatcher W, Santos J, Silvestre F, Kim I, Staples C (2010). "Perspective on physiological⁄endocrine and nutritional factors influencing fertility in post-partum dairy cows". Reprod Dom Anim. 45: 2–14. doi:10.1111/j.1439-0531.2010.01664.x. 
  26. Jump up ^ Surai PF, Karadas F, Pappas A, Sparks N (2006). "Effect of organic selenium in quail diet on its accumulation in tissues and transfer to the progeny". Br Poult Sci. 47: 65–72. doi:10.1080/00071660500475244. 
  27. Jump up ^ Navas-Carretero S, Cuervo M, Abete I, Zulet M, Martinez J (2010). "Frequent consumption of selenium-enriched chicken meat by adults causes weight loss and maintains their antioxidant status". Biol Trace Elem Res. 143: 8–19. doi:10.1007/s12011-010-8831-x. 
  28. Jump up ^ Fisinin V, Papazyan T, Surai PF (2009). "Producing selenium-enriched eggs and meat to improve the selenium status of the general population". Crit Rev Biotech. 29: 18–28. doi:10.1080/07388550802658030. 
  29. Jump up ^ Mahan D. Organic selenium fed to swine - its potential impact on human health issues. In: Midwest Swine Nutrition Conference. Indianapolis, IN, 2005.
  30. Jump up ^ Sel-Plex receives authorisation [online]. Available at: http://www.allaboutfeed.net/news/sel-plex-receives-authorisation-id98.html. Accessed January 21.
  31. Jump up ^ Commission of the European Communities. Commission regulation (EC) No 1750/2006 of 27 November 2006 concerning the authorisation of selenomethionine as a feed additive [online]. Available at: http://eur-lex.europa.eu/LexUriServ/LexUriServ.do?uri=OJ:L:2006:330:0009:0011:EN:PDF. Accessed January 21.
  32. Jump up ^ Organic Materials Review Institute. Sel-Plex [online]. Available at: http://www.omri.org/simple-opl-search/results/sel-plex. Accessed January 21.
  33. Jump up ^ European Food Safety Authority (2006). "Opinion of the scientific panel on additives and products or substances used in animal feed on the safety and efficacy of the product Sel-Plex®2000 as a feed additive according to regulation (EC) No 1831/2003". EFSA Journal. 348: 1–40. 
  34. Jump up ^ Rayman M, Infante H, Sargent M (2008). "Food-chain selenium and human health: spotlight on speciation". Br J Nutr. 100: 238–253. doi:10.1017/s0007114508922522. 
  35. Jump up ^ Connolly C, Power R, Hynes M (2004). "Validation of method for total selenium determination in yeast by flame atomic absorption spectrometry". Biol Trace Elem Res. 100: 87–94. doi:10.1385/bter:100:1:087. 
  36. Jump up ^ European Food Safety Authority. Selenium-enriched yeast as source for selenium added for nutritional purposes in foods for particular nutritional uses and foods (including food supplements) for the general population: Scientific opinion of the panel on food additives, flavourings, processing aids and materials in contact with food. EFSA Journal 2008;766:1-42.
  37. Jump up ^ B'Hymer C, Caruso J (2006). "Selenium speciation analysis using inductively coupled plasma-mass spectrometry". J Chrom A. 1114: 1–20. doi:10.1016/j.chroma.2006.02.063. 
  38. Jump up ^ Lobinski R, Edmonds J, Suzuki K, Uden P (2000). "Species-selective determination of selenium compounds in biological materials". Pure Appl Chem. 72: 447–461. doi:10.1351/pac200072030447. 

Misalignment alters gait

The Atlas and the autonomic nervous system

(parasympathetic nervous system)

nervi
Gastrointestinal disorders, heart arrhythmia, sensation of torpor, sensitivity disorders, chronic fatigue, sleep disorders, malfunctioning of sense organs...
Would you have ever thought that a single bone can be responsible for all these disorders?
Normal movements of the head and body can temporarily compress or lengthen the various vascular, neural and lymphatic structures.
These compressions are temporary and do not entail any problems whatsoever: in fact, the body is made to move.
On the contrary, an Atlas out of alignment causes a constant pressure on the various structures!

Anatomy of the autonomic nervous system

The autonomic nervous system is made of various nerves that run around the Atlas vertebra. In total, there are 12 pairs of cranial nerves arising from the brain and present both on the right side and left side.
The vagus nerve, or tenth cranial nerve, is the longest and most important nerve of the parasympathetic nervous system (it belongs to the neurovegetative system) as it regulates the functions of almost all of the internal organs. The vagus nerve innervates the larynx, the pharynx, the upper part of the oesophagus, the part of the external hearing apparatus, the heart, the lungs, the stomach, the intestine and even several muscles.
vagus
The accessory nerve, known as the eleventh cranial nerve, is a motor nerve, that regulates the muscular activity. Among the various muscles controlled by the accessory nerve there is the trapezius muscle (musculus trapezius) and the sternocleidomastoid muscle (musculus sternocleidomastoideus) or SCM.
The glossopharyngeal nerve, known as the ninth cranial nerve, is the nerve that carries signals from the back of the tongue to the brain and innervates the muscles of the pharynx. It is important for swallowing and in activating the parotid gland.
The three cranial nerves described above come down from the cranium through the jugular foramen, which is right in front of the Atlas. It is exactly in this narrow passage that something basically unknown to traditional medicine occurs: that is, the malposition of the Atlas which can cause a pressure on the above mentioned nerves triggering pains that doctors fail to explain.
But there is good news: with one single treatment the malposition of the Atlas can be resolved.

Effects of the malposition of the Atlas on the nervous system

clessidra gialla
An Atlas out of alignment:
  1. can narrow the passage between the vertebral channel and the sinus at the base of the cranium, reducing the space available for the spinal marrow. This alters or blocks the flow of electrochemical impulses;
  2. can cause pressure on various nerves: glossopharyngeal nerve, vagus nerve, accessory nerve and occipital nerve;
  3. can disturb the flow of cerebrospinal fluid in the vertebral channel. This fluid, known simply as liquor, has the function to nourish, protect and pad the marrow;
  4. can create a muscoloskeletal unbalance, which leads to the hardening of various muscles and thus to the compression of the nerves coming out of vertebras C5, C6 and C7. Since said nerves innervate the arms, their compression produces a feeling of torpor in the hands or fingers (paraesthesias).

Further effects on the nervous system

An Atlas out of alignment, besides producing consequences on the autonomic nervous system, can have negative effects also on the peripheral nervous system causing, for example, the peripheral nerve compression syndrome. When nerves are compressed by particularly hardened muscular chains other painful phenomena can occur, such as the sciatic nerve compression syndrome.
In this case, the contracted piriformis muscle pushes down on the sciatic nerve thus producing pain in the gluteal area and in the the back of the legs, known as sciatica.
Did you know that an Atlas out of alignment can actually cause gluteal neuralgia or numbness of the fingers?
yellow: vagus nerve (Nervus vagus)

Monday, 22 August 2016

5 News Toxic Shock Syndrome posted 5/2015

From Wikipedia, the free encyclopedia
Jump to: navigation, search

Toxic shock syndrome
Classification and external resources
ICD-10A48.3
ICD-9040.82
DiseasesDB13187
MedlinePlus000653
eMedicinemed/2292 emerg/600 derm/425 ped/2269
MeSHD012772
Toxic shock syndrome (TSS) is a potentially fatal illness caused by a bacterial toxin. Different bacterial toxins may cause toxic shock syndrome, depending on the situation. The causative bacteria include Staphylococcus aureus, where TSS is caused by enterotoxin type B or TSST-1, and Streptococcus pyogenes, where it is caused by streptococcal pyrogenic exotoxins. Streptococcal TSS is sometimes referred to as toxic shock-like syndrome (TSLS) or streptococcal toxic shock syndrome (STSS).


Signs and symptoms[edit]

Symptoms of toxic shock syndrome vary depending on the underlying cause. TSS resulting from infection with the bacterium Staphylococcus aureus typically manifests in otherwise healthy individuals with high fever, accompanied by low blood pressure, malaise and confusion, which can rapidly progress to stupor, coma, and multiple organ failure. The characteristic rash, often seen early in the course of illness, resembles a sunburn, and can involve any region of the body, including the lips, mouth, eyes, palms and soles. In patients who survive the initial phase of the infection, the rash desquamates, or peels off, after 10–14 days.
In contrast, TSS caused by the bacterium Streptococcus pyogenes, or TSLS, typically presents in people with pre-existing skin infections with the bacteria. These individuals often experience severe pain at the site of the skin infection, followed by rapid progression of symptoms as described above for TSS. In contrast to TSS caused by Staphylococcus, streptococcal TSS less often involves a sunburn-like rash.
For staphylococcal toxic shock syndrome, the diagnosis is based strictly upon CDC criteria defined in 2011, as follows:[1]
  1. Body temperature > 38.9 °C (102.02 °F)
  2. Systolic blood pressure < 90 mmHg
  3. Diffuse macular erythroderma
  4. Desquamation (especially of the palms and soles) 1 – 2 weeks after onset.
  5. Involvement of three or more organ systems:
  6. Negative results of:
Cases are classified as confirmed or probable based on the following:
  • Confirmed: All six of the criteria above are met (unless the patient dies before desquamation can occur)
  • Probable: Five of the six criteria above are met.

Pathophysiology[edit]

In both TSS (caused by S. aureus) and TSLS (caused by S. pyogenes), disease progression stems from a superantigen toxin that allows the nonspecific binding of MHC II with T cell receptors, resulting in polyclonal T cell activation. In typical T cell recognition, an antigen is taken up by an antigen-presenting cell, processed, expressed on the cell surface in complex with class II major histocompatibility complex (MHC) in a groove formed by the alpha and beta chains of class II MHC, and recognized by an antigen-specific T cell receptor.
By contrast, superantigens do not require processing by antigen-presenting cells but instead interact directly with the invariant region[citation needed] of the class II MHC molecule. In patients with TSS, up to 20% of the body's T cells can be activated at one time. This polyclonal T-cell population causes a cytokine storm, followed by a multisystem disease. The toxin in S. aureus infections is TSS Toxin-1, or TSST-1. The TSST-1 is secreted as a single polypeptide chain.
The gene encoding toxic shock syndrome toxin is carried by a mobile genetic element of S. aureus in the SaPI family of pathogenicity islands.[2]

Treatment[edit]

The severity of this disease frequently warrants hospitalization. Admission to the intensive care unit is often necessary for supportive care (for aggressive fluid management, ventilation, renal replacement therapy and inotropic support), particularly in the case of multiple organ failure.[3] The source of infection should be removed or drained if possible: abscesses and collections should be drained. Anyone wearing a tampon at the onset of symptoms should remove it immediately. Outcomes are poorer in patients who do not have the source of infection removed.[3]
Antibiotic treatment should cover both S. pyogenes and S. aureus. This may include a combination of cephalosporins, penicillins or vancomycin. The addition of clindamycin[4] or gentamicin[5] reduces toxin production and mortality.

Prognosis[edit]

With proper treatment, patients usually recover in two to three weeks[citation needed]. The condition can, however, be fatal within hours.

Epidemiology[edit]

Staphylococcal toxic shock syndrome is rare and the number of reported cases has declined significantly since the 1980s. Patrick Schlievert, who published a study on it in 2004, determined incidence at 3 to 4 out of 100,000 tampon users per year; the information supplied by manufacturers of sanitary products such as Tampax and Stayfree puts it at 1 to 17 of every 100,000 menstruating people per year.[6][7]
The CDC has stopped tracking TSS. However, there was a rise in reported cases in the early 2000s: eight deaths from the syndrome in California in 2002 after three successive years of four deaths per year, and Schlievert's study found cases in part of Minnesota more than tripled from 2000 to 2003.[6] Schlievert considers earlier onset of menstruation to be a cause of the rise; others, such as Philip M. Tierno and Bruce A. Hanna, blame new high-absorbency tampons introduced in 1999 and manufacturers discontinuing warnings not to leave tampons in overnight.[6]

History[edit]

Initial description[edit]

The term toxic shock syndrome was first used in 1978 by a Denver pediatrician, James K. Todd, to describe the staphylococcal illness in three boys and four girls aged 8–17 years.[8] Even though S. aureus was isolated from mucosal sites in the patients, bacteria could not be isolated from the blood, cerebrospinal fluid, or urine, raising suspicion that a toxin was involved. The authors of the study noted reports of similar staphylococcal illnesses had appeared occasionally as far back as 1927, but the authors at the time failed to consider the possibility of a connection between toxic shock syndrome and tampon use, as three of the girls who were menstruating when the illness developed were using tampons. Many cases of TSS occurred after tampons were left in the person using them.[9]

Rely tampons[edit]

Following controversial test marketing in Rochester, New York and Fort Wayne, Indiana,[10] in August 1978, Procter and Gamble introduced superabsorbent Rely tampons to the United States market[11] in response to women's demands for tampons that could contain an entire menstrual flow without leaking or replacement.[12] Rely used carboxymethylcellulose (CMC) and compressed beads of polyester for absorption. This tampon design could absorb nearly 20 times its own weight in fluid.[13] Further, the tampon would "blossom" into a cup shape in the vagina to hold menstrual fluids without leakage.
In January 1980, epidemiologists in Wisconsin and Minnesota reported the appearance of TSS, mostly in those menstruating, to the CDC.[14] S. aureus was successfully cultured from most of the subjects. The Toxic Shock Syndrome Task Force was created and investigated the epidemic as the number of reported cases rose throughout the summer of 1980.[15] In September 1980, CDC reported users of Rely were at increased risk for developing TSS.[16]
On 22 September 1980, Procter and Gamble recalled Rely[17] following release of the CDC report. As part of the voluntary recall, Procter and Gamble entered into a consent agreement with the FDA "providing for a program for notification to consumers and retrieval of the product from the market."[18] However, it was clear to other investigators that Rely was not the only culprit. Other regions of the United States saw increases in menstrual TSS before Rely was introduced.[19]
It was shown later that higher absorbency of tampons was associated with an increased risk for TSS, regardless of the chemical composition or the brand of the tampon. The sole exception was Rely, for which the risk for TSS was still higher when corrected for its absorbency.[20] The ability of carboxymethylcellulose to filter the S. aureus toxin that causes TSS may account for the increased risk associated with Rely.[13]

Notable cases[edit]

See also[edit]

References[edit]

  1. ^ "Toxic shock syndrome (other than Streptococcal) (TSS): 2011 Case Definition". Centers for Disease Control and Prevention. May 8, 2014. Retrieved August 17, 2014. 
  2. ^ Lindsay, JA; Ruzin, A; Ross, HF; Kurepina, N; Novick, RP (July 1998). "The gene for toxic shock toxin is carried by a family of mobile pathogenicity islands in Staphylococcus aureus". Molecular microbiology 29 (2): 527–43. doi:10.1046/j.1365-2958.1998.00947.x. PMID 9720870. 
  3. ^ a b Zimbelman J, Palmer A, Todd J (1999). "Improved outcome of clindamycin compared with beta-lactam antibiotic treatment for invasive Streptococcus pyogenes infection". Ped Infect Dis J 18 (12): 1096–1100. doi:10.1097/00006454-199912000-00014. 
  4. ^ Schlievert PM, Kelly JA (1984). "Clindamycin-induced suppression of toxic-shock syndrome-associated exotoxin production". J Infect Dis 149 (3): 471. doi:10.1093/infdis/149.3.471. PMID 6715902. 
  5. ^ van Langevelde P, van Dissel JT, Meurs CJ, Renz J, Groeneveld PH (1 August 1997). "Combination of flucloxacillin and gentamicin inhibits toxic shock syndrome toxin 1 production by Staphylococcus aureus in both logarithmic and stationary phases of growth". Antimicrob Agents Chemother 41 (8): 1682–5. PMC 163985. PMID 9257741. 
  6. ^ a b c Lyons, Julie Sevrens (25 January 2005). "A New Generation Faces Toxic Shock Syndrome". The Seattle Times. Knight Ridder Newspapers.  first published as "Lingering Risk," San Jose Mercury News, December 13, 2004
  7. ^ "Stayfree — FAQ About Toxic Shock Syndrome (TSS)". 2006. Retrieved 2006-10-13. 
  8. ^ Todd J, Fishaut M, Kapral F, Welch T (1978). "Toxic-shock syndrome associated with phage-group-I staphylococci". Lancet 2 (8100): 1116–8. doi:10.1016/S0140-6736(78)92274-2. PMID 82681. 
  9. ^ Todd J (1981). "Toxic shock syndrome—scientific uncertainty and the public media". Pediatrics 67 (6): 921–3. PMID 7232057. 
  10. ^ Finley, Harry. "Rely Tampon: It Even Absorbed the Worry!". Museum of Menstruation. Retrieved 2006-03-20. 
  11. ^ Hanrahan S; Submission, Haworth Continuing Features (1994). "Historical review of menstrual toxic shock syndrome". Women Health 21 (2–3): 141–65. doi:10.1300/J013v21n02_09. PMID 8073784. 
  12. ^ Citrinbaum, Joanna (Oct 14, 2003). "The question's absorbing: 'Are tampons little white lies?'". The Digital Collegian. Retrieved 2006-03-20. 
  13. ^ a b Vitale, Sidra (1997). "Toxic Shock Syndrome". Web by Women, for Women. Archived from the original on 2006-03-16. Retrieved 2006-03-20. 
  14. ^ CDC (23 May 1980). "Toxic-shock syndrome—United States". MMWR Morb Mortal Wkly Rep 29 (20): 229–230. 
  15. ^ Dennis Hevesi (September 10, 2011). "Bruce Dan, Who Helped Link Toxic Shock and Tampons, Is Dead at 64". New York Times. Retrieved 2011-09-12. Dr. Bruce Dan, who as a leading federal researcher helped establish a link between the life-threatening disease toxic shock syndrome and the use of tampons, prompting a major shift in the way tampons are produced, died Tuesday in Baltimore. He was 64. 
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