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  • Chowcb123's Avatar
    17 posts since Sep '17
  • Chowcb123's Avatar
    17 posts since Sep '17
    • To Damienfeath, f your mum cb ok. You know the meaning of considerate or not. CB kia, want smoke go find somewhere far from human civilisation and smoke to your death ok. It's because sg have more such ppl from 3rd countries and they breed their disgusting filths into this world that make living damn depressing in sg. Still want others to tell you nicely. That guy should whack you with the pole. MF.

  • lemon1974's Avatar
    9,238 posts since Dec '04
    • it seem like AMDEP are starting to do some minor redeployment for those services under seletar package.. 

      SBS3472 on 76 for one week on same slot, 3518/3482 are also alway spotted on sv76 recently. 

      SBS3517 spotted on amdep service as well. cant  remember what service.

      SG1173 is on sv269 as well for one week (same timing). no perm sticker on coinbox.

       

  • Chowcb123's Avatar
    17 posts since Sep '17
  • lemon1974's Avatar
    9,238 posts since Dec '04
  • Chowcb123's Avatar
    17 posts since Sep '17
  • azharjj's Avatar
    6,417 posts since Aug '07
    • Originally posted by SMB315C:

      SG5513S - SG5515L
      >> SMRT as of today

      whats the previous operator?

  • carbikebus's Avatar
    19,744 posts since Nov '03
    • Originally posted by SMB315C:

      SG5513S - SG5515L
      >> SMRT as of today

      No wonder saw this trio at BKE yesterday..I got post under redeployment thread yesterday.

  • Chowcb123's Avatar
    17 posts since Sep '17
  • SMB315C's Avatar
    1,883 posts since Sep '14
    • Originally posted by TIB 585L:

      911 suspect change 2 AP SD to 2 S SD

      3085X 1742Z not doing 911 AP anymore

      Counted 4 SDs with 6 bendies on 911

      They also added another 1 S shift to 911..

  • SMB315C's Avatar
    1,883 posts since Sep '14
  • Chowcb123's Avatar
    17 posts since Sep '17
  • bic_cherry's Avatar
    414 posts since Jul '05
    • zhihau (SBY) wroteIt's not as simple as input vs output kind of thing. Here's an analogy.

      You pump petrol in a car and it drives the car engine, the car moves. Just as it's like our bodies, the food we eat fuels our activities. The car is made up of many small parts which are subjected to wear and tear and may break down. Our bodies are made up of many cells, each cell having many chemical pathways and influence surrounding cells by biochemical signaling. The downstream cascade may go haywire.

      The choice of petrol can be high octane or low octane, the car can still break down for some funny reasons, just as how we get diabetes despite our high calorie or low calorie diets. It's more of understanding the process of pancreas producing and secreting insulin and glucagon and how these processes help moderate blood glucose levels.

      Genetic disposition, stress levels, diseases can all have a hand in causing diabetes. Pinning the blame squarely on the diet is not correct and very irresponsible.


      Of course it is primarily a CALORIC input and output issue. Every fat(adipose) and muscle cell has a finite limit where caloric content is concerned and any further increase would mandate creation of more fat cells since muscle mass is unlikely to increase without strength training or aerobic exercise .

      Thus the resistance to insulin due to already energy saturated cells.

      With insufficient demand for energy expenditure due to sedentary lifestyles, the pancreas has no choice but to go into overdrive to lower blood glucose levels because high blood glucose is TOXIC to cells (inflammation of blood vessels is what causes heart attacks (atherosclerosis), blindness, kidney failure, amputation etc). High insulin levels can also promote cancer because insulin and human growth hormone have similar origins/function.

      Finally, the system breaks down, firstly due to high blood glucose causing damage to the pancreas itself amongst others, secondarily due to overworked pancreas, fatigued to the point of failure due to the insulin production overdrive.

      Thus, diabetes is indeed a disease caused by caloric consumption being in excess of caloric expenditure resulting in all the excess energy accumulation in the body causing damage everywhere inside (just like how u damage a lithium battery when u charge it to ABOVE capacity).

      For those economically inclined, diabetes is simply a failure of caloric economics with the excess calories causing havoc being too much to properly be absorbed by cells already at their maximum caloric storage limit.

  • Chowcb123's Avatar
    17 posts since Sep '17
  • Chowcb123's Avatar
    17 posts since Sep '17
    • More NSF deaths like Gavin...All sweep under the carpet by simpky saying bionix overturned and Gavin found beside. Real reasons of cockups, sop, fuckup officers etc never reported.

  • Yokkie's Avatar
    12 posts since Sep '17
    • Just see how long he can tahan bah... I think should be quite hard for him though. But,  I'd he really loves u,  he will respect whatever your decision

  • Moderator
    Aik TC's Avatar
    1,532 posts since Jun '10
    • How an American Countess became a Buddhist nun and helped spread feminism in Sri Lanka

      Vinod Moonesinghe 10 September Scroll.in

      Miranda Maria Banta later adopted the Bahaii faith, and died a Hindu.

      In March 1896, in the San Francisco suburb of Oakland, the Sri Lankan Buddhist revivalist and missionary Hewavitarne Dharmapala, on a lecture tour of the United States, met Countess Canavarro. Seeking spiritual sustenance, she struck him as determined and forceful. According to Tessa Bartholomeusz, four months after meeting her, Dharmapala proposed that she travel to Sri Lanka and establish an order of Buddhist “nuns”, and become full-time principal of the island’s first Buddhist girls’ high school, Sanghamitta, named for the first female Buddhist missionary to Sri Lanka.

      On the evening of August 30, 1897, at the New Century Hall on New York’s Fifth Avenue, Dharmapala administered to the Countess Canavarro the five Buddhist precepts (pansil), making her the first female convert to Buddhism on American soil. Thus, she became the first in a new order of “Buddhist nuns” which Dharmapala wanted to create in Sri Lanka, some seven centuries after female ordination died out. She took on the enormously significant religious moniker “Sister Sanghamitta”, recalling the ancient missionary, as well as the school she intended to run.

      According to Thomas A Tweed, the Countess, by the very act of conversion, caused a huge stir. In the rigidly Christian atmosphere of fin de siecle America, adopting another religion simply was not done. Although almost forgotten in the US, in her day, she made a considerable impact on the spread of Buddhism, Bahaism, Hinduism, and esoterica in general.

      Her effect on Sri Lanka, despite her short stay of three years, has been much greater. Her school still exists as Sri Sanghamitta Balika Vidyalaya, Punchi Borella, an offshoot of the co-educational Mahabodhi vernacular school resurrected by Dharmapala at Foster Lane. Her imaginings of what a Buddhist nun should be have had their effect on the order of Dasa Sil Mathas, even their attire being based on her original design.

      Sanghamitta Convent

      Sanghamitta Girls’ School had a short but chequered history. Founded by the Women’s Education Society in 1891, its first principal, an Australian woman called Kate Pickett, drowned. Louisa Roberts, a local teacher, acted as a stop-gap until Marie Musaeus Higgins, a German-American, arrived. In 1893, the latter broke away and started her own school, Musaeus College. Thereafter, Kate Pickett’s mother, Elise, served as school director, returning to Australia just before the Countess arrived.

      Dharmapala and the Countess wanted to establish Sanghamitta on the lines of a Roman Catholic convent school, with Buddhist nuns teaching the girls. Accordingly, the school was relocated from its existing location, Tichbourne Hall, and moved to the same location as the “convent” – the Sanghamitta Upasikaramaya. Dharmapala and the Countess decided on Gunter House, a single-storey building set amidst a hectare of gardens in Darley Lane (now Foster Lane), which the Maha Bodhi Society bought for 25,000 Sri Lankan rupees (30 million in today’s currency).

      The convent, school, and an orphanage were soon up and running, large crowds attending the opening. There was no shortage of pupils for the school. The Countess, who styled herself as Mother Superior, came to be known by the children as Nona Amma (or Madam mother). Sister Dhammadinna (a Burgher woman called Sybil LaBrooy) managed the household, and several Sinhalese “nuns” completed the staff.

      In mid-1898, Catherine Shearer, a nurse from Boston’s Eliot Hospital, joined her, becoming “Head Sister” Padmavatie. However, the two did not get along. The Countess expected Shearer to run things for her, while she busied herself with Mahabodhi Society work.

      This friction between them betokened a deeper difference in attitudes. According to Bartholomeusz, the Countess considered Shearer “a dreamer”, but herself remained ignorant of the discipline expected from a Buddhist nun. Much against his will, she accompanied Dharmapala to Kolkata and appears, at some point, to have tried to seduce him. Finally, she removed herself from Gunther House and set up a convent on her own. This not only proved unsuccessful but also doomed the Sanghamitta Convent.

      Countess Canavarro

      As an infant, Miranda Maria Banta, born in 1849 in East Texas, accompanied her mother to California. At 17, she married post master, insurance agent and scalp-hunter Samuel Cleghorn Bates, having four children by him. Bartholomeusz thinks he may have been an abusive husband, leading her to leave him.

      She probably met Lieutenant António de Souza Canavarro, scion of a noble family, on his way to become the Portuguese consul general in Hawaii – then an independent country – in August 1882. By November the next year, she styled herself “Miranda A de Souza Canavarro”.

      A figure in West Coast high society, her conversion to Buddhism attracted considerable publicity.

      Even the obscure Gazette Appeal of Marion County, Georgia, reported it:

      “This convert, whose purpose is to devote years of labor in the far east to uplift her sex, is the Countess M. De Canavarro, an American, formerly of San Francisco, who, to follow her chosen life surrenders, as the officiating priest announced, family, fortune, and title.”

      Years later, the whiff of scandal remained. The Iowa-based newspaper Adair County Democrat claimed Dharmapala had hypnotised her and prevailed upon her to desert her family.

      Companionate marriage

      In November 1900, after the Sanghamitta Convent debacle, the Countess returned to the US, moving to the East Coast. She lectured on Buddhism and the Orient in general, and several of her lectures were published.

      Soon after, she entered a companionate marriage with a fellow Theosophist, Myron H Phelps, a patent lawyer. The couple travelled to Sri Lanka posing as brother and sister. However, she continued describing herself as a Buddhist “nun”.

      In December 1902, the Countess accompanied Phelps to Akka in Palestine, to meet Abbas Effendi, the Bahai leader. The Countess interviewed Abbas’ sister Behiah Khanum, who provided the biographical material which went into Phelps’ book Life and Teachings of Abbas Effendi. In late 1903, still bearing the name “Sister Sanghamitta”, she declared her acceptance of the Bahai faith.

      Two years later, she and Phelps were to play host to the influential Hindu revivalist and moderniser Ponnambalam Ramanathan and his Australian secretary, Lillie Harrison, who would later become Ramanathan’s wife and take on the name Leelawathy. Ramanathan’s intellectual view of Hinduism attracted Phelps: by 1908, he would see himself as a Hindu.

      Phelps left the Countess, journeying to India to join the independence movement. Almost bankrupt, she moved to a farm in Blackstone, Virginia, in a compassionate marriage with Deuel Sperry, the longest-lasting of her relationships. She continued to lecture, but concentrated on writing: she produced several novels and the autobiographical Insight into the Far East.

      In 1922, she moved back to Hawaii, settling later in the Los Angeles suburb of Glendale, from where she would travel to the Ananda Ashrama, founded by Swami Paramananda in nearby La Crescenta. For, in the last phase of her life, she adopted Vedanta Hinduism. She passed away in Glendale on July 25, 1933.

      The Countess’ Legacy

      Her legacy affected not only the future of Eastern religion in the United States, but also the development of Buddhism, which had already arrived in the country along with the Chinese who flooded into California with the 1849 Gold Rush. The Countess represented a different type of Buddhist.

      Even more profoundly, her example affected the way in which Sri Lankan society looked at women. Hitherto, crushed by Victorian values, the female gender were considered nothing more than sexual playthings or baby-making machines. According to Bartholomeusz:

      “The Countess and her ‘sisters’, by choosing to become world-renouncers, challenged the stereotype of the pious Buddhist woman as wife and mother; they helped to make renunciation a respectable choice for Buddhist women in Ceylon.”

      Despite the Buddha’s teaching enhancing the position of women, stressing the ability of women to achieve enlightenment and the existence of female arhants, later accretions to the canon made out that the feminine body proved a barrier to understanding the Dhamma. The Sri Lankan Buddhist tradition had, for seven centuries, lacked a female branch of the Sangha. This reinforced the idea of women being mentally inferior to their male counterparts, which became dogma.

       

      Countess Canavarro, by resurrecting the image of the Buddhist woman seeking enlightenment, demonstrated the intellectual equality of genders and overthrew this perspective. Her action proved vital to the development of feminism on this island.

  • iveco's Avatar
    17,026 posts since Mar '04
    • Originally posted by array88:

      Not all past services were withdrawn because of low demand... Many were due to duplication with MRT (even when they had sufficient demand), mergers/amendments with other services that are later proven to be unwise or no longer effective today, or even for the purpose of forcing people to switch to other underutilized bus svcs/MRT lines.

      And note that loading patterns / route planning decades ago may not be the same as today, considering new MRT lines, increase in population (hence limitation of MRT's capacity) and especially new estates/flats. So some services with low demand in the past may do pretty well today.

      14 and 51 are classic examples of merged entities that ended up being too long for their own good.

  • laurence82's Avatar
    124,804 posts since Nov '03
    • someone jump down from my block

      early in the morning

       

      actually i read report somewhere that suicidal people tend to commit suicide after midnight or early in the morning

      cant remember the rationale why, maybe coz nighttime cannot sleep then hu si luan xiang

  • TehJarVu's Avatar
    117,149 posts since Dec '03
  • Moderator
    H2 Chemistry @ BedokFunland JC (near VJC & TJC)
    UltimaOnline's Avatar
    13,373 posts since May '05
  • Moderator
    H2 Chemistry @ BedokFunland JC (near VJC & TJC)
    UltimaOnline's Avatar
    13,373 posts since May '05
    • [Medicine / Chemistry / Biology ] - You gotta respect the marvelous biochemical-metabolic-genetic design intelligence of the human body*, in this example, using one equilibria system (ie. conjugate acid-base pair of Taurine) to control the pH gradient within mitochondria, in turn to shift the position of equilibrium thermodynamically favorably for a separate biochemical equilibria system : a redox equilibria (since the pH directly affects reduction and oxidation potentials as predicted by Le Chatelier's principle) between the NADH / NAD+ conjugate redox pair and the GSH / GSSG conjugate redox pair (ie. reduced and oxidized forms of the anti-oxidant Glutathione, the functional adequacy of which is in turn correlated with MTHFR gene polymorphisms), for the tricarboxylic acid cycle, the electron transport chain, the proton and electrical gradients and subsequent oxidative phosphorylation and ATP-production by ATP synthase (note : the formation of ATP from ADP and Pi by itself is endergonic, ie. thermodynamically unfeasible with a positive Gibbs free energy change, unless coupled during cellular respiration to the electrochemical gradient created by the difference in proton molarity across the mitochondrial membrane, making the overall coupled reaction exergonic, ie. thermodynamically feasible with a negative Gibbs free energy change.)

      * Both the religious-inclined and the atheistic-inclined will no doubt seize upon such examples to egregiously claim rigorous support for each of their own Intelligent-Design-Creator-Creationism and Natural-Selection-Darwinism-Evolution beliefs respectively, but both would be equally inadequate, and would behoove a separate discussion for another day.

      _____________________________________________________________

      "Taurine, glutathione and bioenergetics" by Hansen SH, Grunnet N.

      Biochemistry textbook presentations of bioenergetics and mitochondrial function normally focus on the chemiosmotic theory with introduction of the tricarboxylic acid cycle and the electron transport chain, the proton and electrical gradients and subsequent oxidative phosphorylation and ATP-production by ATP synthase. The compound glutathione (GSH) is often mentioned in relation to mitochondrial function, primarily for a role as redox scavenger. Here we argue that its role as redox pair with oxidised glutathione (GSSG) is pivotal with regard to controlling the electrical or redox gradient across the mitochondrial inner-membrane. The very high concentration of taurine in oxidative tissue has recently led to discussions on the role of taurine in the mitochondria, e.g. with taurine acting as a pH buffer in the mitochondrial matrix. A very important consequence of the slightly alkaline pH is the fact that the NADH/NAD(+) redox pair can be brought in redox equilibrium with the GSH redox pair GSH/GSSG.An additional consequence of having GSH as redox buffer is the fact that from the pH dependence of its redox potential, it becomes possible to explain that the mitochondrial membrane potential has been observed to be independent of the matrix pH. Finally a simplified model for mitochondrial oxidation is presented with introduction of GSH as redox buffer to stabilise the electrical gradient, and taurine as pH buffer stabilising the pH gradient, but simultaneously establishing the equilibrium between the NADH/NAD(+) redox pair and the redox buffer pair GSH/GSSG.

      https://www.ncbi.nlm.nih.gov/pubmed/23392865

      Edited by UltimaOnline 21 Sep `17, 7:15AM
  • Moderator
    H2 Chemistry @ BedokFunland JC (near VJC & TJC)
    UltimaOnline's Avatar
    13,373 posts since May '05
    • [Medicine / Chemistry / Biology ] - You gotta respect the marvelous biochemical-metabolic-genetic design intelligence of the human body*, in this example, using one equilibria system (ie. conjugate acid-base pair of Taurine) to control the pH gradient within mitochondria, in turn to shift the position of equilibrium thermodynamically favorably for a separate biochemical equilibria system : a redox equilibria (since the pH directly affects reduction and oxidation potentials as predicted by Le Chatelier's principle) between the NADH / NAD+ conjugate redox pair and the GSH / GSSG conjugate redox pair (ie. reduced and oxidized forms of the anti-oxidant Glutathione, the functional adequacy of which is in turn correlated with MTHFR gene polymorphisms), for the tricarboxylic acid cycle, the electron transport chain, the proton and electrical gradients and subsequent oxidative phosphorylation and ATP-production by ATP synthase (note : the formation of ATP from ADP and Pi by itself is endergonic, ie. thermodynamically unfeasible with a positive Gibbs free energy change, unless coupled during cellular respiration to the electrochemical gradient created by the difference in proton molarity across the mitochondrial membrane, making the overall coupled reaction exergonic, ie. thermodynamically feasible with a negative Gibbs free energy change.)

      * Both the religious-inclined and the atheistic-inclined will no doubt seize upon such examples to egregiously claim rigorous support for each of their own Intelligent-Design-Creator-Creationism and Natural-Selection-Darwinism-Evolution beliefs respectively, but both would be equally inadequate, and would behoove a separate discussion for another day.

      _____________________________________________________________

      "Taurine, glutathione and bioenergetics" by Hansen SH, Grunnet N.

      Biochemistry textbook presentations of bioenergetics and mitochondrial function normally focus on the chemiosmotic theory with introduction of the tricarboxylic acid cycle and the electron transport chain, the proton and electrical gradients and subsequent oxidative phosphorylation and ATP-production by ATP synthase. The compound glutathione (GSH) is often mentioned in relation to mitochondrial function, primarily for a role as redox scavenger. Here we argue that its role as redox pair with oxidised glutathione (GSSG) is pivotal with regard to controlling the electrical or redox gradient across the mitochondrial inner-membrane. The very high concentration of taurine in oxidative tissue has recently led to discussions on the role of taurine in the mitochondria, e.g. with taurine acting as a pH buffer in the mitochondrial matrix. A very important consequence of the slightly alkaline pH is the fact that the NADH/NAD(+) redox pair can be brought in redox equilibrium with the GSH redox pair GSH/GSSG.An additional consequence of having GSH as redox buffer is the fact that from the pH dependence of its redox potential, it becomes possible to explain that the mitochondrial membrane potential has been observed to be independent of the matrix pH. Finally a simplified model for mitochondrial oxidation is presented with introduction of GSH as redox buffer to stabilise the electrical gradient, and taurine as pH buffer stabilising the pH gradient, but simultaneously establishing the equilibrium between the NADH/NAD(+) redox pair and the redox buffer pair GSH/GSSG.

      https://www.ncbi.nlm.nih.gov/pubmed/23392865

      Edited by UltimaOnline 21 Sep `17, 7:15AM
  • BusAnalayzer's Avatar
    10,312 posts since May '12
    • Originally posted by Travellator:

      Loading level of Svc 55 (DD) from Upp East Coast Ter  @ 2:31pm (30/08/17 Sunday) Off Peak, Bus in front = 9min, Bus behind = 17min

       

      Upp East Coast Ter -- 2(0/2)

      Upp East Coast Rd -- 3(0/1) *all other b/s no pax boarding/alighting activity

      Bedok South Ave 1 -- no pax boarding/alighting activity

      Marine Parade Rd -- 4(0/1), 5(0/1), 7(0/2)

      Still Rd -- 9(0/2), 10(0/1), 10(-1/1)

      Jln Eunos -- 10(-5/5), 9(-1/0) *2nd highest pax boarding/alighting activity occured at Eunos MRT

      HG Ave 3 -- 8(-1/0), 7(-2/1), 6(-1/0), 4(-2/0)

      HG Ave 2 -- 2(-3/1), 4(0/2)

      AMK Ave 3 -- 4(-1/1), 7(0/3), 9(0/2), 8(-2/1)

      AMK Ave 10 -- 19(-1/12), 18(-6/5), 20(-1/3) *I alighted here @ 3:31pm (60min used)

       

      *Off peak demand is very weak throughout the route, maybe due to front bus only 9 min apart. Demand only start to pick up significantly at AMK Ave 10.

      *Highest loading = 20 pax occured at AMK Ave 10 at the bus stop I alighted. Therefore we can see that most ppl take this route for travelling to Bishan MRT from nearby AMK estate. This is also due to less bus svc in AMK Ave 10 (only svc 45 and 55).

      I guess peak hour weekday demand should be way better??

       

      Firstly, I have to say nice to see you here. Your style on loading analysis is pretty similar to mine. Well drafted. 

      I have two cents to offer - It would be productive and worthwhile if you did the loading analysis on weekdays AM and PM peak rather than off-peak. You can never judge any service by its off-peak loading. 

      svc 55 ofcourse on weekdays peak is packed between Bishan and Eunos. Towards Eunos, its loading also depends on if 25/854 is right in front. The Still - Marine Parade - UEC mostly has weak loading.

  • Moderator
    H2 Chemistry @ BedokFunland JC (near VJC & TJC)
    UltimaOnline's Avatar
    13,373 posts since May '05
    • As the following medical study illustrates, the link between Taurine and heart disease is complex. In some cases, heart disease is indicated by unusually high Taurine levels (regardless of supplementation); while in other cases, heart disease is indicated by unusually low Taurine levels (regardless of supplementation).

      Medical science is complex, because human biology, human chemistry and human genetics are complex. So while Taurine (or any supplement, for that matter) certainly isn't a magic bullet nor even necessarily helpful (depending on your genetics and exact underlying medical condition, it may or may not be helpful); notwithstanding, self-education is your own responsibility (do your own online research to see if Taurine, or any other supplement for that matter, is worth your trying it out). At the same time, as the adage advises, while knowledge can be empowering, a little knowledge is a dangerous thing. So always proceed in life with sensible caution.

      Decreased Myocardial Taurine Levels and Hypertaurinuria in a Kindred with Mitral-Valve Prolapse and Congestive Cardiomyopathy

      http://www.nejm.org/doi/full/10.1056/NEJM198101153040301#t=articleTop

      Excerpt :

      Our study suggests that hypertaurinuria is associated with low levels of taurine in the myocardium, one type of the mitral-valve-prolapse syndrome, and a form of congestive cardiomyopathy. Hypertaurinuria may also account for the relatively rapid development of congestive cardiomyopathy in the two subjects with initially uncomplicated mitral-valve prolapse. It is also not clear whether the depressed myocardial taurine levels are etiologically related to the two heart diseases, whether all three disorders are coincidental genetic accidents, or whether the depressed myocardial taurine concentration is the cause of congestive cardiomyopathy alone and is unrelated to mitral-valve prolapse. The available evidence favors the hypothesis that all three problems are related.

      Regardless of the extent of the possible interrelation, one additional point is evident: the syndrome of mitral-valve prolapse, with all its clinical and echocardiographic features, was not caused by mucinous transformation, scalloping of the mitral leaflets, or elongation of the chordae tendineae. Rather, a pathologic process in the papillary muscles seems to be the underlying cause — an interpretation that supports the view that mitral-valve prolapse is a syndrome with diverse causes.

      Taurine (2-aminoethanesulfonic acid) is the most abundant free amino acid in the heart, accounting for more than half the total free amino acid pool. Circulating taurine derived from either dietary sources or from biosynthetically active tissues is taken up at various sites, particularly in cardiac and skeletal muscle. The rate of turnover of taurine in normal myocardium is extremely slow, with a half-life of approximately 15 days. Cardiac taurine levels are unchanged by a pyridoxine-deficient diet, fasting, or taurine loading; however, taurine concentrations rise in failing or hypertrophied myocardial tissue.

      Loss of cardiac-muscle taurine has been demonstrated in left-ventricular tissue of anesthetized dogs in which ischemia was induced by occlusion of the coronary artery; in the absence of fibrosis, loss occurred as early as four hours after occlusion in one study and at 16 hours in another. In the family members in our study who were patients, however, there was no evidence of extramural or intramural narrowing of the coronary artery in the cardiac tissue in which myocardial taurine levels were depressed. Furthermore, there was no clinical evidence of ischemic heart disease in these patients.

      On the other hand, studies in animals and one study of human myocardium at autopsy have both shown moderate to marked elevation of taurine levels in failing or hypertrophied hearts; this elevation was also present in the controls with cardiomyopathy in our study. However, family members with congestive cardiomyopathy had abnormally low levels of myocardial taurine in failing hearts. It therefore appears that at least some of these family members have an unusual combination of features: an absence of myocardial infarction in the presence of myocardial taurine levels that were abnormally low, particularly in comparison with levels found in other studies suggesting that myocardial taurine is elevated in congestive heart failure, perhaps as a compensatory positive inotropic mechanism.

      Although a direct causal relation cannot yet be firmly established, it seems likely that in subjects described in this study, clinical and echocardiographic features of mitral-valve prolapse were produced by an early, localized cardiomyopathy in the papillary muscles that was associated with a depressed myocardial taurine concentration and eventual myocardial fibrosis. The congestive cardiomyopathy probably represents an extension of the local process to more or all of the remaining myocardium.

      http://www.nejm.org/doi/full/10.1056/NEJM198101153040301#t=articleTop

      Edited by UltimaOnline 22 Sep `17, 2:25AM