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Twins are two offspring produced by the same pregnancy.[1] Twins can either be monozygotic ("identical"), meaning that they can develop from just one zygote that will then split and form two embryos, or dizygotic ("fraternal"), meaning that they can develop from two different eggs, each are fertilized by separate sperm cells.[2]
In contrast, a fetus which develops alone in the womb is called a singleton, and the general term for one offspring of a multiple birth is multiple.[3]
- 1 Statistics
- 2 Zygosity
- 3 Degree of separation
- 4 Demographics
- 5 Delivery interval
- 6 Complications during pregnancy
- 7 Management of birth
- 8 Human twin studies
- 9 Language development
- 10 Other animals
- 11 See also
- 12 References
- 13 Further reading
- 14 Foundations
The twin birth rate in the United States rose 76% from 1980 through 2009, from 18.9 to 33.3 per 1,000 births.[4] The Yoruba have the highest rate of twinning in the world, at 45–50 twin sets (or 90–100 twins) per 1,000 live births,[5][6][7] possibly because of high consumption of a specific type of yam containing a natural phytoestrogen which may stimulate the ovaries to release an egg from each side.[8][9]
In Central Africa there are 18–30 twin sets (or 36–60 twins) per 1,000 live births.[10] In Latin America, South Asia, and Southeast Asia, the lowest rates are found; only 6–9 twin sets per 1,000 live births. North America and Europe have intermediate rates of 9–16 twin sets per 1,000 live births.[10]
Multiple pregnancies are much less likely to carry to full term than single births, with twin pregnancies lasting only 37 weeks (3 weeks less than full term) on average.[11]
Women who have a family history of fraternal twins have a higher chance of producing fraternal twins themselves, as there is a genetically linked tendency to hyper-ovulate. There is no known genetic link for identical twinning.[12] Other factors that increase the odds of having fraternal twins include maternal age, fertility drugs and other fertility treatments, nutrition, and prior births.[13]
Zygosity is the degree of identity in the genome of twins. There are five common variations of twinning.
The three most common variations are all dizygotic (fraternal):[14]
- Male–female twins are the most common result, 50 percent of dizygotic twins and the most common grouping of twins.
- Female–female dizygotic twins (sometimes called "sororal twins")
- Male–male dizygotic twins
The other two variations are monozygotic ("identical") twins:[14]
- Female–female monozygotic twins
- Male–male monozygotic twins (less common)
Among non-twin births, male singletons are slightly (about five percent) more common than female singletons. The rates for singletons vary slightly by country. For example, the sex ratio of birth in the US is 1.05 males/female,[15] while it is 1.07 males/female in Italy.[16] However, males are also more susceptible than females to die in utero, and since the death rate in utero is higher for twins, it leads to female twins being more common than male twins.
Dizygotic (fraternal) twins
Dizygotic (DZ) or fraternal twins (also referred to as "non-identical twins", "dissimilar twins", "biovular twins", and, informally in the case of females, "sororal twins") usually occur when two fertilized eggs are implanted in the uterus wall at the same time. When two eggs are independently fertilized by two different sperm cells, fraternal twins result. The two eggs, or ova, form two zygotes, hence the terms dizygotic and biovular. Fraternal twins are, essentially, two ordinary siblings who happen to be born at the same time, since they arise from two separate eggs fertilized by two separate sperm, just like ordinary siblings. Instead of fraternal twins, this situation can also occasionally result in a chimera, someone colloquially described as their own fraternal twin.
Dizygotic twins, like any other siblings, have an extremely small chance of having the same chromosome profile. Even if they happen to have the same chromosome profile, they will always have different genetic material on each chromosome, due to chromosomal crossover during meiosis. Like any other siblings, dizygotic twins may look similar, particularly given that they are the same age. However, dizygotic twins may also look very different from each other. They may be of different sexes or the same sex, just like ordinary siblings.
Studies show that there is a genetic basis for dizygotic twinning. However, it is only the mother who has any effect on the chances of having such twins; there is no known mechanism for a father to cause the release of more than one ovum. Dizygotic twinning ranges from six per thousand births in Japan (similar to the rate of monozygotic twins) to 14 and more per thousand in some African countries.[8]
Dizygotic twins are also more common for older mothers, with twinning rates doubling in mothers over the age of 35.[17] With the advent of technologies and techniques to assist women in getting pregnant, the rate of fraternals has increased markedly.
Monozygotic (identical) twins
Monozygotic (MZ) or identical twins occur when a single egg is fertilized to form one zygote (hence, "monozygotic") which then divides into two separate embryos.
Regarding spontaneous or natural monozygotic twinning, a recent theory proposes that monozygotic twins are formed after a blastocyst essentially collapses, splitting the progenitor cells (those that contain the body's fundamental genetic material) in half, leaving the same genetic material divided in two on opposite sides of the embryo. Eventually, two separate fetuses develop.[18] Spontaneous division of the zygote into two embryos is not considered to be a hereditary trait, but rather a spontaneous or in some cases a random event.[17][19]
Monozygotic twins may also be created artificially by embryo splitting. It can be used as an expansion of IVF to increase the number of available embryos for embryo transfer.[20]
Monozygotic twinning occurs in birthing at a rate of about three in every 1000 deliveries worldwide.[19]
The likelihood of a single fertilization resulting in monozygotic twins is uniformly distributed in all populations around the world.[17] This is in marked contrast to dizygotic twinning, which ranges from about six per thousand births in Japan (almost similar to the rate of identical twins, which is around 4–5) to 15 and more per thousand in some parts of India[21] and up to over 20 in some Central African countries.[10] The exact cause for the splitting of a zygote or embryo is unknown.
In vitro fertilization (IVF) techniques are more likely to create dizygotic twins. For IVF deliveries, there are nearly 21 pairs of twins for every 1,000.[22]
Genetic and epigenetic similarity
Monozygotic twins are genetically nearly identical and they are always the same sex unless there has been a mutation during development. The children of monozygotic twins test genetically as half-siblings (or full siblings, if a pair of monozygotic twins reproduces with another pair or with the same person), rather than first cousins. Identical twins do not have the same fingerprints, due to the fact that even in a small space inside the womb, people have contact with different parts of this environment, which gives small variations in the same digital, making them unique.[23] Monozygotic twins always have different phenotypes. Normally due to an environmental factor or the deactivation of different X chromosomes in female monozygotic twins, and in some extremely rare cases, due to aneuploidy, twins may express different sexual phenotypes, normally from an XXY Klinefelter syndrome zygote splitting unevenly.[24][25][26]
Monozygotic twins, although genetically very similar, are not genetically exactly the same. The DNA in white blood cells of 66 pairs of monozygotic twins was analyzed for 506,786 single nucleotide polymorphisms known to occur in human populations. Polymorphisms appeared in 2 of the 33 million comparisons, leading the researchers to extrapolate that the blood cells of monozygotic twins may have on the order of one DNA-sequence difference for every 1.2 x 107 nucleotides, which would imply hundreds of differences across the entire genome.[27] The mutations producing the differences detected in this study would have occurred during embryonic cell-division (after the point of fertilization). If they occur early in fetal development, they will be present in a very large proportion of body cells.
Another cause of difference between monozygotic twins is epigenetic modification, caused by differing environmental influences throughout their lives. Epigenetics refers to the level of activity of any particular gene. A gene may become switched on, switched off, or could become partially switched on or off in an individual. This epigenetic modification is triggered by environmental events. Monozygotic twins can have markedly different epigenetic profiles. A study of 80 pairs of monozygotic twins ranging in age from three to 74 showed that the youngest twins have relatively few epigenetic differences. The number of epigenetic differences increases with age. Fifty-year-old twins had over three times the epigenetic difference of three-year-old twins. Twins who had spent their lives apart (such as those adopted by two different sets of parents at birth) had the greatest difference.[28] However, certain characteristics become more alike as twins age, such as IQ and personality. This phenomenon illustrates the influence of genetics in many aspects of human characteristics and behavior.[29][30][31]
A 1981 study of a deceased triploid XXX twin fetus without a heart showed that although its fetal development suggested that it was an identical twin, as it shared a placenta with its healthy twin, tests revealed that it was probably a polar body twin. The authors were unable to predict whether a healthy fetus could result from a polar body twinning.[32] In 2003, a study argued that many cases of triploidity arise from semi-identical twinning.[33] In 2007, a study reported a case of a pair of living twins, one intersex and one a phenotypical male. The twins were both found to be chimeras and to share all of their maternal DNA but only half of their father's DNA. The exact mechanism of fertilization could not be determined but the study stated that it was unlikely to be a case of polar body twinning.[34]
Degree of separation
The degree of separation of the twins in utero depends on if and when they split into two zygotes. Dizygotic twins were always two zygotes. Monozygotic twins split into two zygotes at some time very early in the pregnancy. The timing of this separation determines the chorionicity (the number of placentae) and amniocity (the number of sacs) of the pregnancy. Dichorionic twins either never divided (i.e.: were dizygotic) or they divided within the first 4 days. Monoamnionic twins divide after the first week.
In very rare cases, twins become conjoined twins. Furthermore, there can be various degrees of shared environment of twins in the womb, potentially leading to pregnancy complications.
It is a common misconception that two placentas means twins are dizygotic. But if monozygotic twins separate early enough, the arrangement of sacs and placentas in utero is indistinguishable from dizygotic twins.
| Normally, twins have two separate (di- being a numerical prefix for two) chorions and amniotic sacs, termed Dichorionic-Diamniotic or "DiDi". It occurs in almost all cases of dizygotic twins (except in very rare cases of fusion between their blastocysts[35] ) and in 18–36%[36] (or around 25%[35]) of monozygotic (identical) twins.
DiDi twins have the lowest mortality risk at about 9 percent, although that is still significantly higher than that of singletons.[37]
|Dichorionic-Diamniotic twins form when splitting takes place by the third day after fertilization.[35]
| Monochorionic twins share the same placenta.
Monochorionic twins generally have two amniotic sacs (called Monochorionic-Diamniotic "MoDi"), which occurs in 60–70% of the pregnancies with monozygotic twins,[36] and in 0.3% of all pregnancies.[38] Monochorionic-Diamniotic twins are almost always monozygotic, with a few exceptions where the blastocysts have fused.[35]
Monochorionic twins share the same placenta, and thus have a risk of twin-to-twin transfusion syndrome.
|Days 4-8
|Monochorionic twins share the same amnion in 1–2% of monozygotic twin pregnancies.[36]
Monoamniotic twins are always monozygotic.[39]
The survival rate for monoamniotic twins is somewhere between 50%[39] to 60%.[40]
Monoamniotic twins, as with diamniotic monochorionic twins, have a risk of twin-to-twin transfusion syndrome. Also, the two umbilical cords have an increased chance of being tangled around the babies. Because of this, there is an increased chance that the newborns may be miscarried or suffer from cerebral palsy due to lack of oxygen.
|Monoamniotic twins occur when the split takes place after the ninth day after fertilization.[35]
|Conjoined twins
When the division of the developing zygote into 2 embryos occurs, 99% of the time it is within 8 days of fertilization.
Mortality is highest for conjoined twins due to the many complications resulting from shared organs.
|If the division of the zygote occurs later than the 12 days then conjoined twins are usually the result.
- Dichorionic twins with heart activity at 8w5d since co-incubation.gif
Dichorionic-diamniotic twins at 8 weeks and 5 days since co-incubation as part of IVF. The twin at left in the image is shown in the sagittal plane with the head pointing towards upper left. The twin at right in the image is shown in the coronal plane with the head pointing rightwards.
- Monoamniotic twins at 15 weeks.jpg
Abdominal ultrasonography of monoamniotic twins at a gestational age of 15 weeks. There is no sign of any membrane between the fetuses. A coronal plane is shown of the twin at left, and a sagittal plane of parts of the upper thorax and head is shown of the twin at right.
A 2006 study has found that insulin-like growth factor present in dairy products may increase the chance of dizygotic twinning. Specifically, the study found that vegan mothers (who exclude dairy from their diets) are one-fifth as likely to have twins as vegetarian or omnivore mothers, and concluded that "Genotypes favoring elevated IGF and diets including dairy products, especially in areas where growth hormone is given to cattle, appear to enhance the chances of multiple pregnancies due to ovarian stimulation."[41]
From 1980 to 1997, the number of twin births in the United States rose 52%.[42] This rise can at least partly be attributed to the increasing popularity of fertility drugs like Clomid and procedures such as IVF, which result in multiple births more frequently than unassisted fertilizations do. It may also be linked to the increase of growth hormones in food.[41]
About 1 in 90 human births (1.1%) results from a twin pregnancy.[43] The rate of dizygotic twinning varies greatly among ethnic groups, ranging as high as about 45 per 1000 births (4.5%) for the Yoruba to 10% for Linha São Pedro, a tiny Brazilian settlement which belongs to the city of Cândido Godói.[44] In Cândido Godói, one in five pregnancies has resulted in twins.[45] The Argentine historian Jorge Camarasa has put forward a theory that experiments of the Nazi doctor Josef Mengele could be responsible for the high ratio of twins in the area.[46] His theory was rejected by Brazilian scientists who had studied twins living in Linha São Pedro; they suggested genetic factors within that community as a more likely explanation.[47] A high twinning rate has also been observed in other places of the world, including :
- Igbo-Ora in Nigeria[48]
- Kodinji, located in Kerala, India[49]
- Mohammadpur Umri, located in Uttar Pradesh, India[50][51][52]
The widespread use of fertility drugs causing hyperovulation (stimulated release of multiple eggs by the mother) has caused what some call an "epidemic of multiple births". In 2001, for the first time ever in the US, the twinning rate exceeded 3% of all births. Nevertheless, the rate of monozygotic twins remains at about 1 in 333 across the globe.
In a study on the maternity records of 5750 Hausa women living in the Savannah zone of Nigeria, there were 40 twins and 2 triplets per 1000 births. Twenty-six percent of twins were monozygotic. The incidence of multiple births, which was about five times higher than that observed in any western population, was significantly lower than that of other ethnic groups, who live in the hot and humid climate of the southern part of the country. The incidence of multiple births was related to maternal age but did not bear any association to the climate or prevalence of malaria.[53][54]
Predisposing factors
The predisposing factors of monozygotic twinning are unknown.
Dizygotic twin pregnancies are slightly more likely when the following factors are present in the woman:
- She is of West African descent (especially Yoruba)
- She is between the age of 30 and 40 years
- She is greater than average height and weight
- She has had several previous pregnancies.
Women undergoing certain fertility treatments may have a greater chance of dizygotic multiple births. In the United States it has been estimated that by 2011 36% of twin births resulted from conception by assisted reproductive technology.[55]
The risk of twin birth can vary depending on what types of fertility treatments are used. With in vitro fertilisation (IVF), this is primarily due to the insertion of multiple embryos into the uterus. Ovarian hyperstimulation without IVF has a very high risk of multiple birth. Reversal of anovulation with clomifene (trade names including Clomid) has a relatively less but yet significant risk of multiple pregnancy.
Delivery interval
A 15-year German study[56] of 8,220 vaginally delivered twins (that is, 4,110 pregnancies) in Hesse yielded a mean delivery time interval of 13.5 minutes.[57] The delivery interval between the twins was measured as follows:
- Within 15 minutes: 75.8%
- 16-30 minutes: 16.4%
- 31-45 minutes: 4.3%
- 46-60 minutes: 1.7%
- Over 60 minutes: 1.8% (72 instances)
The study stated that the occurrence of complications "was found to be more likely with increasing twin-to-twin delivery time interval" and suggested that the interval be kept short, though it noted that the study did not examine causes of complications and did not control for factors such as the level of experience of the obstetrician, the wish of the women giving birth, or the "management strategies" of the procedure of delivering the second twin.
Complications during pregnancy
Vanishing twins
Researchers suspect that as many as 1 in 8 pregnancies start out as multiples, but only a single fetus is brought to full term, because the other has died very early in the pregnancy and has not been detected or recorded.[58] Early obstetric ultrasonography exams sometimes reveal an "extra" fetus, which fails to develop and instead disintegrates and vanishes. This is known as vanishing twin syndrome. Also, in an unknown proportion of cases, two zygotes may fuse soon after fertilization, resulting in a single chimeric embryo, and, later, fetus.
Conjoined twins
Conjoined twins (or the commonly used term "siamese") are monozygotic twins whose bodies are joined together during pregnancy. This occurs when the zygote starts to split after day 12[35] following fertilization and fails to separate completely. This condition occurs in about 1 in 50,000 human pregnancies. Most conjoined twins are now evaluated for surgery to attempt to separate them into separate functional bodies. The degree of difficulty rises if a vital organ or structure is shared between twins, such as the brain, heart or liver.
A chimera is an ordinary person or animal except that some of their parts actually came from their twin or from the mother. A chimera may arise either from monozygotic twin fetuses (where it would be impossible to detect), or from dizygotic fetuses, which can be identified by chromosomal comparisons from various parts of the body. The number of cells derived from each fetus can vary from one part of the body to another, and often leads to characteristic mosaicism skin coloration in human chimeras. A chimera may be intersex, composed of cells from a male twin and a female twin. In one case DNA tests determined that a woman, mystifyingly, was not the mother of two of her three children; the mother was found to be a chimera and those of her cells tested happened to derive from one of the fused twins, while two of the children were derived from eggs derived from cells from the other twin making up their mother.[59]
Parasitic twins
Sometimes one twin fetus will fail to develop completely and continue to cause problems for its surviving twin. One fetus acts as a parasite towards the other. Sometimes the parasitic twin becomes an almost indistinguishable part of the other, and sometimes this needs to be treated medically.
Partial molar twins
A very rare type of parasitic twinning is one where a single viable twin is endangered when the other zygote becomes cancerous, or molar. This means that the molar zygote's cellular division continues unchecked, resulting in a cancerous growth that overtakes the viable fetus. Typically, this results when one twin has either triploidy or complete paternal uniparental disomy, resulting in little or no fetus and a cancerous, overgrown placenta, resembling a bunch of grapes.
Miscarried twin
Occasionally, a woman will suffer a miscarriage early in pregnancy, yet the pregnancy will continue; one twin was miscarried but the other was able to be carried to term. This occurrence is similar to the vanishing twin syndrome, but typically occurs later, as the twin is not reabsorbed.
Low birth weight
Twins typically suffer from the lower birth weights and greater likelihood of prematurity that is more commonly associated with the higher multiple pregnancies.
Twin-to-twin transfusion syndrome
Monozygotic twins who share a placenta can develop twin-to-twin transfusion syndrome. This condition means that blood from one twin is being diverted into the other twin. One twin, the 'donor' twin, is small and anemic, the other, the 'recipient' twin, is large and polycythemic. The lives of both twins are endangered by this condition.
Management of birth
For otherwise healthy twin pregnancies where both twins are head down a trial of vaginal delivery is recommended at between 37 and 38 weeks.[60][61] Vaginal delivery in this case does not worsen the outcome for the infant as compared with Caesarean section.[60] There is controversy on the best method of delivery were the first twin is head first and the second is not.[60] When the first twin is not head down a C-section is often recommended.[60] It is estimated that 75% of twin pregnancies in the United States were delivered by Cesarean section in 2008.[62] In comparison, the rate of Cesarean section for all pregnancies in the general population varies between 14% and 40%.[63]
Human twin studies
Twin studies are utilized in an attempt to determine how much of a particular trait is attributable to either genetics or environmental influence. These studies compare monozygotic and dizygotic twins for medical, genetic, or psychological characteristics to try to isolate genetic influence from epigenetic and environmental influence. Twins that have been separated early in life and raised in separate households are especially sought-after for these studies, which have been used widely in the exploration of human nature. Classical twin studies are now being supplemented with molecular genetic studies which identify individual genes.
Unusual twinnings
Among dizygotic twins, in rare cases, the eggs are fertilized at different times with two or more acts of sexual intercourse, either within one menstrual cycle (superfecundation) or, even more rarely, later on in the pregnancy (superfetation). This can lead to the possibility of a woman carrying fraternal twins with different fathers (that is, half-siblings). This phenomenon is known as heteropaternal superfecundation. One 1992 study estimates that the frequency of heteropaternal superfecundation among dizygotic twins, whose parents were involved in paternity suits, was approximately 2.4%; see the references section, below, for more details.
Dizygotic twins from biracial couples can sometimes be mixed twins, which exhibit differing ethnic and racial features. One such pairing was born in Germany in 2008 to a white father from Germany and a black mother from Ghana.[64][65]
Heterotopic pregnancy is an exceedingly rare type of dizygotic twinning in which one twin implants in the uterus as normal and the other remains in the fallopian tube as an ectopic pregnancy. Ectopic pregnancies must be resolved because they can be life-threatening to the mother. However, in most cases, the intrauterine pregnancy can be salvaged.
Among monozygotic twins, in extremely rare cases, twins have been born with different sexes (one male, one female).[66] When monozygotic twins are born with different sexes it is because of chromosomal defects. There can be monozygotic boy/girl twins if the sex gene of the embryo has an extra x chromosome (the fertilized egg would be an xxy) then when the egg splits, one can have xx (girl) genes and one can have xy (boy) genes. This is rare, but possible. Records show there are only 10 known cases of these type twins. The probability of this is so small that multiples having different sexes is universally accepted as a sound basis for in utero clinical determination that the multiples are not monozygotic. Another abnormality that can result in monozygotic twins of different genders is if the egg is fertilized by a male sperm but during cell division only the X chromosome is duplicated. This results in one normal male (XY) and one female with Turner syndrome (45,X).[67] In these cases, although the twins did form from the same fertilized egg, it is incorrect to refer to them as genetically identical, since they have different karyotypes.
Semi-identical twins
Monozygotic twins can develop differently, due to different genes being activated.[68] More unusual are "semi-identical twins". These "half-identical twins" are hypothesized to occur when an unfertilized egg cleaves into two identical attached ova and which are viable for fertilization. Both cloned ova are then fertilized by different sperm and the coalesced eggs undergo further cell duplications developing as a chimeric blastomere. If this blastomere then undergoes a twinning event, two embryos will be formed, each of which have different paternal genes and identical maternal genes.
This results in a set of twins with identical genes from the mother's side, but different genes from the father's side. Cells in each fetus carry genes from either sperm, resulting in chimeras. This form had been speculated until only recently being recorded in western medicine.[69][70][71]
Mirror image twins
Mirror image twins result when a fertilized egg splits later in the embryonic stage than normal timing, around day 9-12. This type of twinning could exhibit characteristics with reversed asymmetry, such as opposite dominant handedness, dental structure, or even organs (situs inversus).[72] If the split occurs later than this time period, the twins risk being conjoined. There is no DNA-based zygosity test that can determine if twins are indeed mirror image.[73]
Language development
There have been many studies highlighting the development of language in twins compared to single-born children. These studies have converged on the notion that there is a greater rate of delay in language development in twins compared to their single-born counterparts.[74] The reasons for this phenomenon are still in question; however, idioglossia was thought to be the major cause.[75] Idioglossia is defined as a private language that is invented usually by young children, specifically twins. The increased focused communication between two twins may isolate them from the social environment surrounding them. Idioglossia has been found to be a rare occurrence and the attention of scientists has shifted away from this idea. Current research is looking into the impacts of a richer social environment for these twins to stimulate their development of language.[76]
Other animals
Twins are common in many animal species, including cats, sheep, ferrets, giant pandas, dogs, deer, marmosets, and tamarins. The incidence of twinning among cattle is about 1–4%, and research is under way to improve the odds of twinning, which can be more profitable for the breeder if complications can be sidestepped or managed. A female calf that is the twin of a bull becomes partially masculinized and is known as a freemartin.
See also
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- ^ Michael R. Cummings "Human Heredity Principles and issues" pg 104
- ^ "Twins, Triplets, Multiple Births: MedlinePlus". Nlm.nih.gov. Retrieved 2013-09-16.
- ^ Martin, Joyce A.; Hamilton, Brady E.; Osterman, Michelle J.K. "Three Decades of Twin Births in the United States, 1980–2009" [1], National Center for Health Statistics Data Brief, No. 80, January 2012
- ^ Zach, Terence; Arun K Pramanik and Susannah P Ford (2007-10-02). "Multiple Births". WebMD. Retrieved 2008-09-29.
- ^ "Genetics or yams in the Land of Twins?". Independent Online. 2007-11-12. Retrieved 2008-09-29.
- ^ "The Land of Twins". BBC World Service. 2001-06-07. Retrieved 2008-09-29.
- ^ a b O. Bomsel-Helmreich; W. Al Mufti (1995). "The mechanism of monozygosity and double ovulation". In Louis G. Keith, Emile Papierik, Donald M. Keith and Barbara Luke. Multiple Pregnancy: Epidemiology, Gestation & Perinatal Outcome. Taylor and Francis. p. 34. ISBN 1-85070-666-2.
- ^ "What's in a yam? Clues to fertility, a student discovers". 1999. Retrieved 2008-09-29.
- ^ a b c Smits, Jeroen; Christiaan Monden (2011). Newell, Marie-Louise, ed. "Twinning across the Developing World". PLoS ONE (Public Library of Science) 6 (9): e25239. PMC 3182188. PMID 21980404. doi:10.1371/journal.pone.0025239.
- ^ Elliott, JP (December 2008). "Preterm labor in twins and high-order multiples". Clinical Perinatology 34 (4): 599–609. PMID 18063108. doi:10.1016/j.clp.2007.10.004.
Unlike singleton gestation where identification of patients at risk for PTL is often difficult, every multiple gestation is at risk for PTL, so all patients can be managed as being at risk.
- ^ "Probability of having twins hereditary?". Go Ask Alice!. Retrieved 15 March 2012.
- ^ Fitch, Karen. "Ask a Geneticist". Understanding Genetics. Stanford School of Medicine. Retrieved 15 March 2012.
- ^ a b "Identical and Fraternal Twins – Determining Zygosity in Twins". Multiples.about.com. 2013-07-16. Retrieved 2013-09-16.
- ^ "United States: People". The World Factbook. Central Intelligence Agency. 2008-09-04. Retrieved 2008-10-02.
- ^ "Italy: People". The World Factbook. Central Intelligence Agency. 2008-09-04. Retrieved 2008-10-02.
- ^ a b c Bortolus, Renata; Fabio Parazzini; Liliane Chatenoud; Guido Benzi; Massimiliano Maria Bianchi; Alberto Marini (1999). "The epidemiology of multiple births". Human Reproduction Update (European Society of Human Reproduction and Embryology) 5 (2): 179–187. ISSN 1355-4786. PMID 10336022. doi:10.1093/humupd/5.2.179.
- ^ Cheng, Maria; Associated Press (2007-07-03). "Study: Twins form after embryo collapses". USA Today. Retrieved 2008-09-30.
- ^ a b April Holladay (2001-05-09). "What triggers twinning?". WonderQuest. Retrieved 2007-03-22.
- ^ Illmensee K, Levanduski M, Vidali A, Husami N, Goudas VT (February 2009). "Human embryo twinning with applications in reproductive medicine". Fertil. Steril. 93 (2): 423–7. PMID 19217091. doi:10.1016/j.fertnstert.2008.12.098.
- ^ Oleszczuk, Jaroslaw J.; Donald M. Keith, Louis G. Keith and William F. Rayburn (November 1999). "Projections of population-based twinning rates through the year 2100". The Journal of Reproductive Medicine 44 (11): 913–921. PMID 10589400. Retrieved 2008-10-02.
- ^ "Time-lapse recordings reveal why IVF embryos are more likely to develop into twins. Researchers believe the laboratory culture could be the cause" (Press release). European Society of Human Reproduction and Embryology. 2007-07-02. Retrieved 2008-09-30.
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- ^ Edwards, JH; T Dent and J Kahn (June 1966). "Monozygotic twins of different sex". Journal of Medical Genetics 3 (2): 117–123. PMC 1012913. PMID 6007033. doi:10.1136/jmg.3.2.117.
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- ^ "Prenatal diagnosis of heterokaryotypic mosaic twins discordant for fetal sex.". Prenat Diagn 20 (12): 999–1003. Dec 2000. PMID 11113914. doi:10.1002/1097-0223(200012)20:12<999::aid-pd948>3.0.co;2-e.
- ^ Li, Rui et al. (2014). "Somatic point mutations occurring early in development: a monozygotic twin study". Journal of Medical Genetics 51: 28–44. Retrieved 2015-02-15.
- ^ Fraga, Mario F.; Esteban Ballestar, Maria F. Paz, Santiago Ropero, Fernando Setien, Maria L. Ballestar†, Damia Heine-Suñer, Juan C. Cigudosa, Miguel Urioste, Javier Benitez, Manuel Boix-Chornet, Abel Sanchez-Aguilera, Charlotte Ling, Emma Carlsson, Pernille Poulsen, Allan Vaag, Zarko Stephan, Tim D. Spector, Yue-Zhong Wu, Christoph Plass and Manel Esteller (July 2005). "Epigenetic differences arise during the lifetime of monozygotic twins". Proc. Natl. Acad. Sci. U.S.A. 102 (30): 10604–9. PMC 1174919. PMID 16009939. doi:10.1073/pnas.0500398102.
- ^ Segal, Nancy L. (1999). Entwined lives: twins and what they tell us about human behavior. New York: Dutton. ISBN 0-525-94465-6. OCLC 40396458.[page needed]
- ^ Plomin, Robert (2001). Behavioral genetics. New York: Worth Pubs. ISBN 0-7167-5159-3. OCLC 43894450.[page needed]
- ^ Mandler,G. (2001) Apart from genetics: What makes monozygotic twins similar? Journal of Mind and Behavior,22,147-159.
- ^ Bieber, Frederick R.; Walter E. Nance; Cynthia C. Morton; Judith A. Brown; Fay O. Redwine; Robert L. Jordan and T. Mohanakumar (1981-08-14). "Genetic Studies of an Acardiac Monster: Evidence of Polar Body Twinning in Man". Science (American Association for the Advancement of Science) 213 (4509): 775–777. JSTOR 1686613. PMID 7196086. doi:10.1126/science.7196086. Non-identical Monozygotic Twins Lay summary – DevBio: A Companion to Developmental Biology (2006).
- ^ Golubovsky, M.D. (February 2003). "Postzygotic diploidization of triploids as a source of unusual cases of mosaicism, chimerism and twinning". Human Reproduction (Oxford Journals) 18 (2): 236–242. PMID 12571155. doi:10.1093/humrep/deg060. Retrieved 2008-02-29. 'Semi-identical' twins discovered Lay summary – Nature News (2007-03-26).
- ^ Souter, Vivienne L.; Melissa A. Parisi, Dale R. Nyholt, Raj P. Kapur, Anjali K. Henders, Kent E. Opheim, Daniel F. Gunther, Michael E. Mitchell, Ian A. Glass and Grant W. Montgomery (April 2007). "A case of true hermaphroditism reveals an unusual mechanism of twinning". Human Genetics (Berlin / Heidelberg: Springer) 121 (2): 179–185. ISSN 1432-1203. PMID 17165045. doi:10.1007/s00439-006-0279-x. Retrieved 2008-02-29. Semi-identical twins discovered Lay summary – BBC News (2007-02-27).
- ^ a b c d e f Shulman, Lee S.; Vugt, John M. G. van (2006). Prenatal medicine. Washington, DC: Taylor & Francis. p. Page 447. ISBN 0-8247-2844-0.
- ^ a b c Curran, Mark (2005-11-02). "Twinning". Focus Information Technology. Retrieved 2008-10-10.
- ^ Benirschke, Kurt (2004). "Multiple Gestation". In Robert Resnik, Robert K. Creasy and Jay D. Iams. Maternal-Fetal Medicine: Principles and Practice (5th ed.). Philadelphia: W. B. Saunders Company. pp. 55–62. ISBN 0-7216-0004-2.
- ^ Cordero L, Franco A, Joy SD, O'shaughnessy RW (December 2005). "Monochorionic diamniotic infants without twin-to-twin transfusion syndrome". J Perinatol 25 (12): 753–8. PMID 16281049. doi:10.1038/sj.jp.7211405.
- ^ a b Pregnancy-Info -- > Monoamniotic Twins Retrieved on July 9, 2009
- ^ MoMo Twins; Monochorionic Monoamniotic Twins By Pamela Prindle Fierro, About.com. Retrieved on July 9, 2009
- ^ a b Steinman, Gary (May 2006). "Mechanisms of twinning: VII. Effect of diet and heredity on the human twinning rate". J Reprod Med 51 (5): 405–410. PMID 16779988. Retrieved 2008-09-29.
- ^ Martin, Joyce A; Melissa M. Park (1999-09-14). "Trends in Twin and Triplet Births: 1980–97" (PDF). National Vital Statistics Reports (National Center for Health Statistics) 47 (24): 1–17. Retrieved 2008-09-29.
- ^ Asch, Richard H.; John Studd (1995). Progress in Reproductive Medicine Volume II. Informa. ISBN 1-85070-574-7. ISSN 1358-8702. OCLC 36287045.[page needed]
- ^ Matte, U; MG Le Roux, B Bénichou, JP Moisan and R Giugliani (1996). "Study on possible increase in twinning rate at a small village in south Brazil". Acta Genet Med Gemellol (Roma) 45 (4): 431–437. PMID 9181177.
- ^ Nick Evans (21 January 2009). "Nazi Angel of death Josef Mengel created twin town in Brazil". The Telegraph.
- ^ Caroline Iggulden (23 January 2009). "The twins from Brazil". The Sun.
- ^ Linda Geddes: Nazi 'Angel of Death' not responsible for town of twins New Scientist online, 27 January 2009
- ^ "The Land Of Twins". BBC World News. 7 June 2001. Retrieved 2009-08-06.
- ^ "Seeing double: the village in deepest Kerala where twins have taken over". The Independent. 12 May 2009. Retrieved 2009-08-06.
- ^ "A village of twins". http://timesofindia.indiatimes.com. Bennett, Coleman & Co. Ltd. Retrieved 23 October 2014.
- ^ "Twin Capital Of The World". http://www.littleindia.com. 4Skylark.com. Retrieved 23 October 2014.
- ^ "Mohammadpur Umri , THE VILLAGE OF TWINS !!". http://himsamachar.com. Business Directory Plugin. Retrieved 23 October 2014.
- ^ Rehan, N; DS Tafida (November 1980). "Multiple births in Hausa women". Br J Obstet Gynaecol 87 (11): 997–1004. PMID 7437372. doi:10.1111/j.1471-0528.1980.tb04464.x.
- ^ Yoruba Customs and Beliefs Pertaining to Twins. Randafricanart.com. Retrieved on 2013-08-10.
- ^ Kulkarni, A. D.; Jamieson, D. J.; Jones Jr, H. W.; Kissin, D. M.; Gallo, M. F.; MacAluso, M.; Adashi, E. Y. (2013). "Fertility Treatments and Multiple Births in the United States". New England Journal of Medicine 369 (23): 2218–2225. PMID 24304051. doi:10.1056/NEJMoa1301467.
- ^ "Twin-to-twin delivery time interval: influencing factors and effect on short-term outcome of the second twin"; Werner Stein, Björn Misselwitz & Stefan Schmidt; Acta Obstetricia et Gynecologica Scandinavica, 87(3):346-353, 2008.
- ^ There were 836,104 deliveries of babies in Hesse over the 15-year study period, including 11,740 twin pregnancies, of which only 4,110 met the inclusion criteria and hence were examined in the study. The excluded twin pregnancies were in cases of (1) delivery before 34 weeks of gestation; (2) when the first twin was delivered by caesarean section; (3) when either of the twins had died in the womb before the onset of labor; and (4) when the pregnancy had been complicated by fetal malformations or Twin-to-twin transfusion syndrome.
- ^ Gedda, Luigi (1995). "The role of research in twin medicine". In Louis G. Keith, Emile Papiernik, Donald M. Keith and Barbara Luke. Multiple Pregnancy: Epidemiology, Gestation & Perinatal Outcome. Taylor and Francis. pp. 4. ISBN 1-85070-666-2.
- ^ New scientist magazine: The stranger within. 15 November 2003, p34
- ^ a b c d Biswas, A; Su, LL; Mattar, C (Apr 2013). "Caesarean section for preterm birth and, breech presentation and twin pregnancies.". Best practice & research. Clinical obstetrics & gynaecology 27 (2): 209–19. PMID 23062593. doi:10.1016/j.bpobgyn.2012.09.002.
- ^ National Collaborating Centre for Women's and Children's Health (November 2011). "Caesarean section" (PDF). NICE. Royal College of Obstetricians and Gynaecologist. pp. 70–103. Retrieved 12 June 2014.
- ^ Lee HC, Gould JB, Boscardin WJ, El-Sayed YY, Blumenfeld YJ (2011). "Trends in cesarean delivery for twin births in the United States: 1995-2008". Obstet Gynecol 118 (5): 1095–101. PMC 3202294. PMID 22015878. doi:10.1097/AOG.0b013e3182318651.
- ^ Women can choose Caesarean birth - BBC article by James Gallagher. 2011.
- ^ Lovell, Tammy (2008-07-17). "Pictured: Proud parents show off their million-to-one black and white twins". Daily Mail (Associated Newspapers Ltd). Retrieved 2008-10-02.
- ^ Moorhead, Joanna (2011-09-24). "Black and white twins". The Guardian. Retrieved 2012-04-07.
- ^ Schmidt, R; EH Sobel, HM Nitowsky, H Dar and FH Allen Jr (February 1976). "Monozygotic twins discordant for sex". Journal of Medical Genetics 13 (1): 64–68. PMC 1013354. PMID 944787. doi:10.1136/jmg.13.1.64. Retrieved 2008-09-29.
- ^ http://www.twinsmagazine.com/images/zygosityMA03.pdf
- ^ Gilbert, Scott F. (2006). "Non-identical Monozygotic Twins". Developmental biology. Sunderland, Mass: Sinauer Associates. ISBN 0-87893-250-X. OCLC 172964621. Retrieved 2008-09-30.
- ^ Souter, Vivienne L.; Melissa A. Parisi, Dale R. Nyholt, Raj P. Kapur, Anjali K. Henders, Kent E. Opheim, Daniel F. Gunther, Michael E. Mitchell, Ian A. Glass and Grant W. Montgomery (April 2007). "A case of true hermaphroditism reveals an unusual mechanism of twinning". Hum. Genet. 121 (2): 179–85. PMID 17165045. doi:10.1007/s00439-006-0279-x.
- ^ LiveScience Staff (2007-03-26). "Rare Semi-Identical Twins Discovered". Imaginova. Retrieved 2008-10-01.
- ^ Whitfield, John (2007). "'Semi-identical' twins discovered". Nature. doi:10.1038/news070326-1.
- ^ Gedda L, Sciacca A, Brenci G et al. (1984). "Situs viscerum specularis in monozygotic twins". Acta Genet Med Gemellol (Roma) 33 (1): 81–5. PMID 6540028.
- ^ Twins genetics, details of environmental impacts. Proactivegenetics.com. Retrieved on 2013-08-10.
- ^ Thorpe, K (June 2006). "Twin children's language development". Early Human Development 82 (6): 387–395. doi:10.1016/j.earlhumdev.2006.03.012.
- ^ Usher, L (13 October 2000). "Idioglossia". Times Literary Supplement: 24.
- ^ Hayashi, C (2007). "Relationship between Twin Language, Twins' Bond, and Social Competence". Twin research and human genetics.
Further reading
- Bacon, Kate. Twins in Society: Parents, Bodies, Space, and Talk (Palgrave Macmillan; 2010) 221 pages; explores the experience of child twins, adult twins, and parents of twins, with a focus on Britain.
- Nieuwint, Aggie; Rieteke Van Zalen-Sprock, Pieter Hummel, Gerard Pals, John Van Vugt, Hans Van Der Harten, Yvonne Heins and Kamlesh Madan (1999). "'Identical' twins with discordant karyotypes". Prenatal Diagnosis 19 (1): 72–6. PMID 10073913. doi:10.1002/(SICI)1097-0223(199901)19:1<72::AID-PD465>3.0.CO;2-V.
- Wenk RE, Houtz T, Brooks M, Chiafari FA (1992). "How frequent is heteropaternal superfecundation?". Acta geneticae medicae et gemellologiae 41 (1): 43–7. PMID 1488855.
- Girela, Eloy; Jose A. Lorente, J. Carlos Alvarez, Maria D. Rodrigo, Miguel Lorente and Enrique Villanueva (1997). "Indisputable double paternity in dizygous twins". Fertility and Sterility 67 (6): 1159–61. PMID 9176461. doi:10.1016/S0015-0282(97)81456-2.
- Shinwell ES, Reichman B, Lerner-Geva L, Boyko V, Blickstein I (September 2007). ""Masculinizing" effect on respiratory morbidity in girls from unlike-sex preterm twins: a possible transchorionic paracrine effect". Pediatrics 120 (3): e447–53. PMID 17766488. doi:10.1542/peds.2006-3574. Retrieved 2008-10-06.
- Lummaa V, Pettay JE, Russell AF (June 2007). "Male twins reduce fitness of female co-twins in humans". Proceedings of the National Academy of Sciences of the United States of America 104 (26): 10915–20. PMC 1904168. PMID 17576931. doi:10.1073/pnas.0605875104. Retrieved 2008-10-06.
- Schein, Elyse; Paula Bernstein (2007). Identical Strangers: A Memoir of Twins Separated and Reunited. New York: Random House. ISBN 1-4000-6496-1. OCLC 123390922.
- Helle, Samuli; Virpi Lummaa and Jukka Jokela (2004). "Selection for Increased Brood Size in Historical Human Populations" (PDF). Evolution 58 (2): 430–436. PMID 15068359. doi:10.1111/j.0014-3820.2004.tb01658.x. Retrieved 2008-10-02.
- "TWINS Guide to the First Year" (PDF). Fort Collins, Colorado: TWINS Magazine. 2008. Retrieved 2008-10-06.
- Samson, Jennifer. "Facts About Multiples: An Encyclopedia of Multiple Birth Records". Retrieved 2008-10-18.
- Am J Med Genet C Semin Med Genet. 2009 May 15;151C(2):136-41. Not really identical: epigenetic differences in monozygotic twins and implications for twin studies in psychiatry. Haque FN, Gottesman II, Wong AH.
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text:
What, exactly, is a low-emmiting, fuel-efficent vehicle? Can a vehicle park there if it's magn-efficent? And how do you know whether you have one?
This sign should read "Low-Emitting, Fuel-Efficient Vehicle Parking Only."
Sign makers in the United Kingdom are so polite. They are ever so regretful that they must inconvenience you by informing you that this parking area is
unsuitable for HGV's. (In other words—to translate for Americans—don't park your semi here, bub.)
That's a charming sign, but an apostrophe and an "s" signal possession. An "s" alone indicates a plural, and that's what "HGVs" is.
Therefore, the message invites the question, "Unsuitable for HGV's what? Who is HGV?"
It's comforting to know that none customers—I guess that means "no customers"—will be towed away. (Sometimes after I dine at a Mexican restaurant, I feel
like I need to be towed away-or, better yet, hoisted onto a flatbed truck.)
Oh, I get it now: "noncustomers."
What really clinches this failure of a sign is the gratuitous period after "away," and the resulting fragment that follows.
What's a "privae," and how does one park it (or them, as the Latin plural appendage "-ae" seems to indicate)? How kind of the sign maker, by the way, to
refrain from taking up all that space on the weekends with a fleet of privas.
Here, two possessive nouns are rendered erroneously in different ways: They should read "Golfers'" and "Rafters'" (unless, of course, the sign is targeting
a single rafter).
Customer's only what? We expect better of a progressive international grocery store chain. (And "1 hour parking"? I know that commercial advertising is inimical to hyphenation—that is perhaps the most ubiquitous signage
error—but, really, does Whole Foods Market have to be as careless as every other merchant?)
You had to see this one coming: otherwise known as privates parking. (Entrance on Whitley, printing by Witless.)
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subset: commoncrawl


text:
7601 E Frank Lloyd Wright Blvd
Directions Scottsdale, AZ 85260
Internet Prices factor in all available rebates and or incentives for each model. Incentives are OAC and given when meeting all prerequisites for any specific incentive. Please ask your sales professional for additional information!
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text:
Re: Chris Lake
Didn't Andy Page work with Sasha? Top boy on the ivories if I remember and a pretty mean programmer too.
Yea he was knocking out some insanely complex beats before it was just a case of dragging blocks about on Ableton. A lot of respect for his productions.


text:
American President Lines, Ltd.
List of Deals
- 1963 $14,550,000 United States Government Insured Merchant Marine Bonds
- 1966 $20,000,000 United States Government Insured Merchant Marine Bonds
- 1971 $50,300,000 United States Government Insured Merchant Marine Bonds
The origin of American President Lines can be traced to 1900 when Robert Dollar created the Dollar Steamship Lines. Dollar, a U.S. lumber trader, originally began acquiring ships as a means for transporting his lumber to Asia. However, as the years progressed his ships began to transport mail and other cargo. In 1921 Dollar Steamship acquired the Pacific Mail Steamship Company, a firm established in 1848 that owned a fleet of ships to transport passengers, cargo, and mail between the Pacific Coast, Japan, and China. In 1923 the company began the practice of naming its ships after American presidents. Dollar Line purchased five passenger-freight vessels and began round-the-world service in 1926.
The company prospered during the 1920s. By 1925 Dollar Lines enjoyed a near monopoly on U.S. shipping on the Pacific Coast. The Merchant Marine Act of 1928 also added the prospect of even greater profits by providing generous subsidies for carrying mail. This act, however, carried the requirement that the mail be transported in new vessels, so Dollar Lines signed what appeared to be a lucrative contract for transporting mail and borrowed heavily to build six new ships to comply with the agreement. Unfortunately, the timing could not have been worse as the effects of the Great Depression began to leave their mark. Only two of the six ships were completed, and one, the President Hoover, ran aground off the coast of Taiwan and was declared a total loss.
In 1938 the liabilities of Dollar Line exceeded its assets by $6 million. The U.S. Marine Commission judges decided that the company was not financially sound and the U.S. government assumed control. It was then renamed American President Lines.
During World War II, American President Lines served as an agent for the War Shipping administration, overseeing the administration of hundreds of vessels including the company fleet. After the war, the son of Robert Dollar, R. Stanley Dollar, initiated a lawsuit in an attempt to force the government to return the company to the family. A settlement was reached in 1952, when American oilman Robert Davies and a group of investors purchased the company from the U.S. government for $18 million.
In the post-World War II years, American President Lines once again prospered. The company introduced two new liners, the President Cleveland and the President Wilson, in 1947 and eleven more ships between 1952 and 1954. In 1961 the company purchased its first containerized ships, where cargo is packed into containers and transported first on land by train or truck and then loaded onto a cargo ship.
In 1965 American President Lines was merged with and became a subsidiary of Natomas Company, an oil and gas exploration company.
By 1970 American President Lines, like other passenger shipping companies, began to experience a sharp decline in passenger traffic as the result of jet aircraft travel. In the early 1970s, the company discontinued both its passenger services and round-the-world freight shipping to focus on its containerization business and its Pacific and Indian Ocean freight business.
American President Lines was spun off from Natomas in 1983 as an independent, publicly held company. During the 1980s and 1990s the company continued to expand its containerization business. It bought new rail equipment, doubled the size of its Oakland, California port facilities, and launched a door-to-door truckload transportation service for domestic freight.
American President Lines was acquired by Neptune Orient Lines (NOL), a Singapore company, in 1997 in a deal worth $825 million. At the time of the merger, American President Lines had $4.6 billion in assets and seventy-six containerships in its fleet. In 2002 American President Lines operates as APL Ltd., a wholly owned subsidiary of NOL.


text:
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Obesity-hypoventilation syndrome (OHS) is associated with significant morbidity and mortality and requires measurement of arterial pCO2 for diagnosis.
To determine diagnostic predictors of OHS among obese patients with suspected obstructive sleep apnea/hypopnea syndrome (OSAHS).
Retrospective analysis of data on 525 sleep clinic patients (mean age 51.4 ± 12.7 years; 65.7% males; mean BMI 34.5 ± 8.1). All patients had sleep studies, and arterialized capillary blood gases (CBG) were measured in obese subjects (BMI > 30 kg/m2).
Of 525 patients, 65.5% were obese, 37.2% were morbidly obese (BMI > 40 kg/m2); 52.3% had confirmed OSAHS. Hypercapnia (pCO2 > 6 kPa or 45 mm Hg) was present in 20.6% obese and 22.1% OSAHS patients. Analysis of OHS predictors showed significant correlations between pCO2 and BMI, FEV1, FVC, AHI, mean and minimum nocturnal SpO2, sleep time with SpO2 < 90%, pO2, and calculated HCO3 from the CBG. PO2 and HCO3 were independent predictors of OHS, explaining 27.7% of pCO2 variance (p < 0.0001). A calculated HCO3 cutoff > 27 mmol/L had 85.7% sensitivity and 89.5% specificity for diagnosis of OHS, with 68.1% positive and 95.9% negative predictive value.
We confirmed a high prevalence of OHS in obese OSAHS patients (22.1%) and high calculated HCO3 level (> 27 mmol/L) to be a sensitive and specific predictor for the diagnosis of OHS.
Macavei VM; Spurling KJ; Loft J; Makker HK. Diagnostic predictors of obesity-hypoventilation syndrome in patients suspected of having sleep disordered breathing. J Clin Sleep Med 2013;9(9):879-884.
Obesity is now considered a global epidemic, and it is projected that by the year 2025, 36% of females and 47% of males will be obese in the UK.1 A recent US study on obesity epidemic showed a levelling off trend for 2009-2010 compared with 2003-2008, with a prevalence of obesity of 35.5% among adult men and 35.8% among adult women.2 This rise in obesity is likely to lead to an increase in respiratory consequences such as obesity-hypoventilation syndrome (OHS), previously known as Pickwickian syndrome.3 It is defined as a combination of obesity (body mass index [BMI] > 30 kg/m2) and daytime hypercapnia (pCO2 > 45 mm Hg or > 6 kPa) in the absence of other known causes of alveolar hypoventilation.4 Obesity is also a main risk factor for obstructive sleep apnea/hypopnea syndrome (OSAHS). Some studies have found hypercapnia in 10% to 20% of OSAHS patients; however, these studies were limited by small sample size, biased recruitment of patients with COPD or severe obesity, and the exclusive enrollment of one gender group and/or ethnic background.5–7 The exact prevalence of OHS is not known, but it is likely the prevalence is different in unselected OSAHS patients.
Little is known about prevalence of OHS in the obese population, irrespective of OSAHS. Current estimates suggest that around 0.3% to 0.4% of the population may have OHS.8,9 Prevalence of OHS is set to increase with rising obesity; therefore, accurate assessment of prevalence of OHS is critical for planning health services to make provision for this condition. Furthermore, the need for early detection of OHS is clear because delay in diagnosis and treatment is associated with significant morbidity and mortality.10,11 If left untreated, OHS is associated with a mortality of 23% at 18 months following discharge from hospital; adequate treatment of OHS reduces this to 3%. In addition, untreated OHS patients are likely to require invasive mechanical ventilation with longer hospital stay.11
Current Knowledge/Study Rationale: The need for early detection of obesity hypoventilation syndrome (OHS) is clear because delay in the diagnosis and treatment is associated with significant morbidity and mortality. In this study we aimed to determine the prevalence of obesity-hypoventilation syndrome among obese patients with suspected sleep apnea and ascertain the validity of previously reported predictors of OHS.
Study Impact: Our study suggests that a normal calculated HCO3 from the CBG can exclude daytime hypercapnia in obese patients, while an elevated bicarbonate and/or nocturnal hypoxia should prompt further investigation for OHS. Routine measurement of bicarbonate in obese patients with suspected sleep apnea can be a useful screening tool for diagnosis of OHS and/or sleep disordered breathing.
The standard assessment to screen for daytime hypercapnia is measurement of arterial blood gases. Performing this measurement in all obese individuals for diagnosis of OHS has its obvious limitations, in terms of the invasive nature of the test and resources required. Identification of simpler clinical predictors of OHS may help with early diagnosis and management. It has been suggested that obese patients with hypercapnia have higher BMI, more severe OSAHS, and worse restrictive chest wall mechanics than normocapnic obese patients.8 There are no clear thresholds with regard to the above parameters that could guide clinicians in identifying those with hypercapnia. A useful and practical measurement appears to be the bicarbonate level. It is readily available and is less invasive than arterial puncture and therefore an attractive choice as a screening tool for hypercapnia.7,12 However, clinical usefulness of this approach needs further evaluation.
Given the high volume of need for noninvasive ventilation for suspected OHS as a cause of hypercapnic respiratory failure at our institution,13 a quality improvement project was undertaken to systematically identify patients with OHS presenting to the sleep disorders center for evaluation.
In this study we aimed to determine prevalence of OHS among obese patients with suspected OSAHS and to check the validity of previously reported predictors of OHS such as body mass index, sleep apnea, and bicarbonate level.
The study cohort comprised of 525 consecutive patients referred to the sleep clinic at North Middlesex University Hospital, London, UK, between January 2009 and January 2011. They were evaluated according to a specifically designed protocol which included presenting symptoms, past medical history (respiratory, metabolic and cardiovascular comorbidities, smoking status), and demographic details (age, gender, and ethnicity). Subsequent anthropometric measurements such as height, weight, neck size, waist/hip ratio, Mallampati score, Epworth Sleepiness Scale score, and spirometry values were obtained.
Four hundred twenty-five patients underwent limited polygraphy sleep study (Embletta; Stowood Scientific Instruments, Oxford UK), which measured oronasal flow using pressure transducer, thoraco-abdominal movement using respiratory inductance plethysmography (RIP), and nocturnal oxygen saturation and heart rate using pulse oximetry.
One hundred patients underwent home overnight oximetry (Konica-Minolta Pulsox-300i; Stowood Scientific Instruments, Oxford UK), which measured nocturnal oxygen saturation and heart rate.
Capillary blood gases (CBG) were measured only in obese subjects (BMI > 30 kg/m2) to identify the presence of hypercapnia in both patients with and without OSAHS. Earlobe arterialized blood sampling was performed as per method described in the British Thoracic Society (BTS) guidelines.14 CBG measurements were taken between 10:00 and 12:00 in sitting position, following 20 min rest. The earlobe was warmed with a hot compress, and rubefacient cream was used during the resting period. Hypercapnia was defined as pCO2 > 6 kPa (45 mm Hg), and normocapnia as pCO2 ≤ 6 kPa (45 mm Hg). HCO3 level was calculated using the Henderson-Hasselbalch formula from the CBG.
The analysis and interpretation of the polygraphy and oximetry data was performed using proprietary software (Somnologica for Embletta version 5.1.0 and DS-5 version 2.10, Stowood Scientific Instruments, Oxford UK). Spirometry was obtained from all patients (Medisoft Hyp'Air, Pulmolink, Kent UK), along with reference values calculated from patient height, weight, and age using equations from the European Respiratory Society.15
Apnea was defined as a cessation of airflow at the upper airway lasting > 10 seconds. Hypopnea was defined as a decrease in airflow, chest, or abdominal excursions with > 50% associated with oxygen desaturation ≥ 4% below baseline value. The apnea-hypopnea index (AHI) was calculated as the number of apnea and hypopnea episodes per hour of sleep. Patients with an AHI > 5 were diagnosed with obstructive sleep apnea (OSAHS). Severity of OSAHS was scaled according to AHI: mild (5-15), moderate (15-30), and severe (> 30). The oxygen desaturation index (ODI) was calculated by establishing the total number of episodes of significant oxygen desaturation (> 4% fall from baseline) per hour of sleep. ODI and mean oxygen saturation were recorded on portable polygraph or overnight oximeter from all 525 subjects. Minimum nocturnal SpO2, total recording time with SpO2 < 90% (TRT90), percentage of time spent in supine vs non-supine, supine AHI, and apnea index were calculated from the portable polygraphy sleep studies on 425 cases.
Obesity was classified according to World Health Organization (WHO) criteria at BMI > 30 kg/m2 into 3 classes: class 1 (30-34.9), class 2 (35-39.9), and class 3 or morbid obesity (≥ 40). Patients with BMI > 30 kg/m2 and daytime hypercapnia (pCO2 > 6 kPa or 45 mm Hg) were categorized as OHS.
Ethical approval for this study was obtained from National Research Ethics Service Committee (Reference: 11/LO/1891).
Patient's clinical details, physiological measurements, and sleep study findings were entered into Stata 10 software for statistical analysis. Demographic, anthropometric, pulmonary function tests, arterial blood gases, and sleep study data of all obese patients were analyzed. The prevalence of OHS was determined by establishing proportion of patients meeting known criteria for the diagnosis of OHS. First, group comparison analysis was performed between normocapnic versus hypercapnic obese patients using Student t-test, χ2, or Mann-Whitney U test when applicable. Second, univariate analysis between daytime pCO2 and other anthropometric variables (neck size, waist hip ratio, BMI), spirometry values (FEV1, FVC, FEV1/FVC ratio), capillary blood gases (pH, pO2, calculated HCO3) and sleep data (AHI, ODI, mean SpO2, minimum nocturnal SpO2, TRT90, % time in supine position) were calculated using Pearson correlation or Kendall tau test when applicable. Finally, multiple regression analysis was completed taking into account pCO2 as dependent variable and the other parameters who correlated with pCO2 after univariate analysis as independent variables. Statistical significance was set at p < 0.05 (two-tailed).
Of 525 consecutive patients included in the retrospective analysis, mean age ± SD was 51.4 ± 12.7 years, and mean BMI 34.5 ± 8.1 kg/m2; 345 were males (65.7%). A total of 344 patients (65.5%) were obese, of which 128 (37.2%) were morbidly obese with a BMI > 40 kg/m2 as presented in Figure 1. Of 525 subjects, 122 (23.2%) were current smokers, 148 (28.2%) ex-smokers and 255 (48.6%) nonsmokers. Prevalence of airflow obstruction was 9.7% (51/525), defined by FEV1/FVC ratio < 70%. Diabetes prevalence was 17.7% (93/525) in our study population and 60.3% (317/525) had a family history of snoring or sleep apnea. Cardiovascular risk factors such as hypertension 39.81% (209/525) or hypercholesterolemia 36.9% (194/525) were common. Obstructive sleep apnea prevalence among obese patients was 79.9% (275/344 patients with AHI > 5 and symptoms), with mean AHI of 32.5 ± 23.9 and ESS 11.8 ± 5.7. OHS prevalence among OSAHS patients was 61/275 (22.1%). Patients with comorbidities that may cause daytime hypercapnia such as severe COPD (FEV1/FVC ratio < 50%; 4 patients) were excluded from the OHS group. Respiratory (asthma, COPD), metabolic (diabetes, hyperlipidemia) and thyroid comorbidities were more common in OHS group when compared to normocapnic obese patients as described in Table 1.
Study population flow diagram
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Patients comorbidities in OHS versus normocapnic obese group
A total of 71/344 patients (20.6%) fulfilled the OHS criteria of concurrent obesity (BMI > 30 kg/m2) and daytime hypercapnia (pCO2 > 6kPa or 45 mm Hg). Table 2 summarizes differences between obese and nonobese patients. Obese patients were older, with increased anthropometric measurements (neck, waist/hip ratio) and lower spirometry values (FEV1, FVC). Obese patients had significantly higher sleep variables (AHI, ODI), lower oxygen saturation during sleep (mean SpO2, minimum nocturnal SpO2), spending more time with SpO2 below 90%, and less time in supine position.
Clinical characteristics of obese versus non obese patients*
A comparison between obesity hypoventilation patients and normocapnic obese is described in Table 3. Of 344 obese patients, 220 (63.9%) were males. Mean age for obese group ± SD was 52.2 ± 12.4 years. Ethnic distribution showed 257 (74.7%) white, 61 (17.7%) black, 19 (5.5%) Asian, and other 7 (2%). OSAHS (AHI > 5 and symptomatic) was more common in hypercapnic obese patients 85.9 % (61/71) versus normocapnic obese 80.2% (219/273).
Clinical characteristics of normocapnic obese patients versus OHS patients*
Prevalence of daytime hypercapnia increased with BMI as shown in Figure 2; 10.9% (14/128) in class 1 obesity, 20.5% (18/88) in class 2 obesity, and 30.4% (39/128) in morbidly obese patients.
OHS distribution in obese patients
Hypercapnic patients were older, heavier, had lower spirometry values, and experienced more sleep events than normocapnic obese patients. Anthropometric measurements (BMI, neck size, waist hip ratio), pulmonary function volumes (FEV1, FVC), sleep data (ODI, mean SpO2, minimum nocturnal SpO2, TRT90), and CBG data (pH, pO2, pCO2, calculated HCO3) were statistically significant between the 2 groups.
Univariate analysis using Pearson correlation or Kendall tau test showed a significant relationship between pCO2 and BMI (r = 0.187; p = 0.0223), FEV1 (r = -0.271; p = 0.0218), FVC (r = -0.253, p = 0.0328), AHI (r = 0.271; p = 0.0083), mean SpO2 (r = -0.214; p = 0.0091), minimum nocturnal SpO2 (r = -0.248; p = 0.0026), time spent with SpO2 below 90% (TRT90, r = 0.328; p = 0.0014), pO2 (r = -0.389; p = 0.0008), and calculated HCO3 (r = 0.306; p = 0.0093).
The relationship between pCO2 and several OHS predictors was estimated using multiple regression allowing for BMI, FEV1, FVC, AHI, mean SpO2, minimum nocturnal SpO2, TRT90, pO2, and calculated HCO3. This model was overall significant (p = 0.0005), and variables taken into account were responsible for 52.2% of pCO2 variance. Following stepwise multiple regression, pO2, and calculated HCO3 were found to be independent predictors of OHS, explaining 27.7% of pCO2 variance (p < 0.0001).
Logistic regression analysis was used to determine various serum bicarbonate thresholds and their statistical value in detecting daytime hypercapnia as presented in Figures 3 and 4.
Bicarbonate performed well as a diagnostic test, with a curve above 45°, rising steeply close to y-axis then flattening out, with the best cut-off giving high sensitivity and specificity
Receiver operating characteristic (ROC) curve analysis for serum bicarbonate levels was performed using logistic regression
A calculated bicarbonate threshold of 27 mmol/L was the most effective in detecting obesity hypoventilation syndrome, with 85.7% sensitivity and 89.5% specificity as described in Table 4.
Calculated bicarbonate from the CBG cutoff values
We found a high prevalence (20.6%) of daytime hypercapnia (OHS) in obese patients attending our sleep clinic. The prevalence increased with an increase in obesity, from 10.9% in mild obesity to 30.4% in morbid obesity. The high prevalence in OHS obese patients in our study was mainly due to high prevalence of obstructive sleep apnea in our obese and hypercapnic obese patients—80% and 86%, respectively. Therefore overall prevalence of OHS in obese sleep apnea patients (22.1%) was similar to prevalence in obese patients (20.6%). Although 51.4% of our patients (obese and non-obese) were either current smokers or ex-smokers, only 9.7% had evidence of airflow obstruction. Patients with moderate to severe airflow obstruction (FEV1/FVC ratio < 50%) as well other causes of daytime hypercapnia were excluded. This study was performed at an altitude of 57 ft, which is just above sea level. Therefore it is unlikely that respiratory alkalosis secondary to altitude hypoxia could lead to a compensatory bicarbonate production.
The exact prevalence of OHS among the general population is unknown; however, the estimated prevalence among the US obese population is thought to be 0.3%.7,8 At the other extreme, the prevalence of OHS among hospitalized adult patients with a BMI > 35 kg/m2 is high, at 31%.9 Several studies have found that as BMI increased, the OHS prevalence increased significantly up to 48% when the BMI was > 50.5–7,10,16,17,19 In the Asian population, OHS is associated with OSAHS at a lower BMI, mainly due to cephalometric differences, such as narrowing of the oropharynx and inferior displacement of the hyoid bone.24–26 In this study, BMI and several other anthropometric measurements (waist/hip ratio, neck size) registered significantly higher values in OHS group versus normocapnic obese patients. We found a prevalence of OHS among obese patients of 20.6%, increasing to 30.4% in those who were morbidly obese. The association between daytime hypercapnia and obesity can be explained by a higher incidence of severe OSAHS among morbidly obese patients.
Most previous studies have examined the prevalence of OHS in patients attending sleep clinic or patients with a confirmed diagnosis of OSAHS. The prevalence among sleep clinic patients has varied from 10% to 20% in different studies, and much higher in patients with confirmed obstructive sleep apnea from 20% to 30%.5,6,17,21,24 A relatively low prevalence of 9% was seen among Japanese OSAHS patients with a mean age of 48 years and BMI of 29.24 Other studies with more selective inclusion criteria such as patients from one gender or of a distinct ethnic group reported higher prevalence up to 38%.16,18 A high prevalence of OHS in some previous studies could also be due to the inclusion of patients with significant airflow limitation. In this study, the prevalence of OHS among patients with OSAHS was 22.1%. This relatively high prevalence of OHS despite a relatively low average BMI of 34.5 kg/m2 compared to other studies may be explained by a high overall prevalence of OSAHS (80%).
A practical tool used for the screening of OHS when interpreting sleep studies, seems to be the amount of time spent with SpO2 < 90%.27 A recent meta-analysis study showed significantly increased time spent with SpO2 < 90% in OHS versus normocapnic OSAHS patients (56% vs 19%).7 Other authors have found this sleep variable to be an independent predictor for OHS, accounting for 24% variance of pCO2.21 In our study, TRT90 was significantly increased in the OHS group—30% compared to 11.7% in normocapnic obese patients. Sleep data variables (mean SpO2, minimum nocturnal SpO2, and TRT90) showed consistent correlation between severity of nocturnal hypoxia and daytime hypercapnia. In our study, AHI correlated with pCO2 after univariate analysis, and unlike other studies was not found to be an independent predictor for OHS.10,19–21
Although gold standard for diagnosis of OHS remains raised arterial pCO2, an increase in the bicarbonate level due to metabolic compensation of respiratory acidosis has been found to be a sensitive screening tool for daytime hypercapnia.7,27
In our study, bicarbonate level was calculated from the CBG data using arterial pH and pCO2 partial pressure in Henderson-Hasselbalch formula. Previous comparison between measured versus calculated bicarbonate levels in 17,621 samples, has found an R2 value of 0.93, indicating a close relationship between serum and calculated HCO3 values.28
In our study using logistic regression with various thresholds for HCO3, a cutoff value of 27 mmol/L had the highest sensitivity (85.7%) and specificity (89.5%) in detecting OHS.
In a previous study using serum bicarbonate sampling, Mokhlesi et al. found after ROC curve analysis an identical HCO3 threshold of 27 mmol/L to have a sensitivity of 92% and a specificity of 50% in identifying OHS. The authors have suggested using serum bicarbonate in conjunction with other markers of OSAHS severity such as AHI when screening for OHS.27 That study revealed a prevalence of OHS of 20% in sleep apnea patients with a mean BMI of 43 and a mean AHI of 62.27 In our study, we found a similar prevalence of OHS in sleep apnea patients of 22.1%, despite a lower severity of sleep apnea with a mean BMI of 34.5 and a mean AHI of 32.5.
In terms of study limitations, we acknowledge that calculated HCO3 from the CBG using Henderson-Hasselbalch formula is not identical with serum bicarbonate measurements, and a 1 mmol/L variation of in HCO3 can have a significant impact on sensitivity and specificity when screening for OHS. Therefore we recommend serum bicarbonate sampling in conjunction with other clinical markers of nocturnal hypoxia.
Previous studies have confirmed high levels of agreement between serum bicarbonate measurements from venous versus arterial samples, suggesting that venous samples can be an acceptable substitute for arterial measurement in clinical setting.22 However, development of commercially available bicarbonate finger strips may further help with noninvasive screening for daytime hypercapnia, allowing an earlier diagnosis of OHS, especially in primary practice.
Early identification of daytime hypercapnia using simple clinical predictors can avoid invasive arterial blood gas sampling and reduce morbidity and mortality associated with OHS. A normal HCO3 value may exclude daytime hypercapnia, while an elevated bicarbonate and/or nocturnal hypoxia should guide clinicians to look for OHS.
The outcome of this study has changed our clinical practice so that we routinely measure serum bicarbonate level on all obese patients followed by the measurement of capillary blood gas pCO2 in patients with raised HCO3 > 27 mmol/L.
We conclude that routine measurement of serum bicarbonate in obese patients can be a useful screening tool for early diagnosis of OHS and/or sleep disordered breathing.
This was not an industry supported study. The authors have indicated no financial conflicts of interest.
apnea-hypopnea index
body mass index
British Thoracic Society
capillary blood gas
chronic kidney disease
chronic obstructive pulmonary disease
Epworth Sleepiness Scale
forced expiratory volume in 1st second
forced vital capacity
serum/arterial bicarbonate
gastroesophageal reflux disease
ischemic heart disease
oxygen desaturation index
obesity hypoventilation syndrome
obstructive sleep apnea/hypopnea syndrome
respiratory inductance plethysmography
pulse oximeter oxygen saturation
standard deviation
transient ischemic attack
total recording time with SpO2 below 90%
United Kingdom
United States
World Health Organization
The authors thank Jennifer Quinn, Epidemiologist Consultant at London School of Hygiene and Tropical Medicine for useful suggestions. Research work was performed at Sleep and Ventilation Unit, Department of Respiratory Medicine, North Middlesex University Hospital, London, UK.
McPherson K, Marsh T, Brown M, authors. Foresight: Tackling obesities: Future choices - modelling future trends in obesity and their impact on health. 2007. London: Government Office for Sciences. Available from: www.foresight.gov.uk/Obesity/14.pdf.
Flegal KM, Carroll MD, Kit BK, Ogden CL, authors. Prevalence of obesity and trends in the distribution of body mass index among US adults, 1999-2010. JAMA. 2012;307:491–7. [PubMed]
Burwell CS, Robin ED, Whaley RD, Bickelmann AG, authors. Extreme obesity associated with alveolar hypoventilation: a Pickwickian Syndrome. Am J Med. 1956;21:811–8. [PubMed]
Al Dabal L, BaHammam AS, authors. Obesity hypoventilation syndrome. Ann Thorac Med. 2009;4:41–9. [PubMed Central][PubMed]
Kessler R, Chaouat A, Schinkewitch P, et al., authors. The obesity-hypoventilation syndrome revisited: a prospective study of 34 consecutive cases. Chest. 2001;120:369–76. [PubMed]
Laaban J-P, Chailleux E, authors; Observatory Group of ANTADIR. Daytime hypercapnia in adult patients with obstructive sleep apnea syndrome in France, before initiating nocturnal nasal continuous positive airway pressure therapy. Chest. 2005;127:710–5. [PubMed]
Mokhlesi B, Tulaimat A, Faibussowitsch I, Wang Y, Evans A, authors. Obesity hypoventilation syndrome: prevalence and predictors in patients with obstructive sleep apnea. Sleep Breath. 2007;11:117–24. [PubMed]
Kaw R, Hernandez AV, Walker E, Aboussouan L, Mokhlesi B, authors. Determinants of hypercapnia in obese patients with obstructive sleep apnea: a systematic review and meta analysis of cohort studies. Chest. 2009;136:787–96. [PubMed]
Mokhlesi B, Saager L, Kaw RQ, authors. Should we routinely screen for hypercapnia in sleep apnea patients before elective non cardiac surgery? Cleve Clin J Med. 2010;77:60–1. [PubMed]
Quint JK, Ward L, Davison AG, authors. Previously undiagnosed obesity hypoventilation syndrome. Thorax. 2007;62:462–3
Nowbar S, Burkhart KM, Gonzales R, et al., authors. Obesity associated hypoventilation in hospitalised patients: prevalence, impact and outcome. Am J Med. 2004;116:1–7. [PubMed]
Macavei V, Spurling KJ, Makker H, authors. Validation of raised serum bicarbonate for diagnosis of Obesity Hypoventilation Syndrome. Eur Respir J. 2012;40 Suppl.56,569s.
Liddicoat H, Zammitt C, Loft J, Moonsie I, Makker H, authors. The effect of body mass index on outcomes of acute non-invasive ventilation (NIV) in a district general hospital. Thorax. 2010;65:A143.
Guideline for emergency oxygen use in adult patients. Thorax. 2008;63 Suppl VI:vi1–vi68. [PubMed]
Quanjer PH, Tammeling GJ, Cotes JE, Pedersen OF, Peslin R, Yernault J-C, authors. Lung volumes and forced ventilatory flows. Report Working Party Standardization of Lung Function Tests, European Community for Steel and Coal. Official Statement of the European Respiratory Society. Eur Respir J. 1993;6 Suppl. 16:5–40. [PubMed]
Akashiba T, Kawahara S, Kosaka N, Ito D, authors. Determinants of chronic hypercapnia in Japanese men with obstructive sleep apnea syndrome. Chest. 2002;121:415–21. [PubMed]
Golpe R, Jimenez A, Carpizo R, authors. Diurnal hypercapnia in patients with obstructive sleep apnoea syndrome. Chest. 2002;122:1100–1. [PubMed]
Leech JA, Onal E, Baer P, Lopata M, authors. Determinants of hypercapnia in occlusive sleep apnea syndrome. Chest. 1987;92:807–13. [PubMed]
Kawata N, Tatsumi K, Terada J, et al., authors. Daytime hypercapnia in obstructive sleep apnoea syndrome. Chest. 2007;132:1832–8. [PubMed]
Dharmagunawardena R, Zammit C, Makker H, authors. Prevalence and predictors of obesity hypoventilation syndrome. Int J Respir Care. 2011;19–22.
Resta O, Foschino-Barbaro MP, Bonfitto P, et al., authors. Prevalence and mechanisms of diurnal hypercapnia in a sample of morbidly obese subjects with obstructive sleep apnoea. Respir Med. 2000;94:240–6. [PubMed]
Herrington WG, Nye HJ, Hammersley MS, Watkinson PJ, authors. Are arterial and venous samples clinically equivalent for the estimation of pH, serum bicarbonate and potassium concentration in critically ill patients? Diabet Med. 2012;29:32–5. [PubMed]
Verin E, Tardif C, Pasquis P, authors. Prevalence of daytime hypercapnia or hypoxia in patients with OSAS and normal lung function. Respir Med. 2001;95:693–6. [PubMed]
Akashiba T, Akahoshi T, Kawahara S, et al., authors. Clinical characteristics of obesity-hypoventilation syndrome in Japan: a multi-center study. Intern Med. 2006;45:1121–5. [PubMed]
Sakakibara H, Tong M, Matsushita K, Hirata M, Konishi Y, Suetsugu S, authors. Cephalometric abnormalities in non-obese and obese patients with obstructive sleep apnoea. Eur Respir J. 1999;13:403–10. [PubMed]
Yu X, Fujimoto K, Urushibata K, Matsuzawa Y, Kubo K, authors. Cephalometric analysis in obese and nonobese patients with obstructive sleep apnea syndrome. Chest. 2003;124:212–8. [PubMed]
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Kumar V, Karon BS, authors. Comparison of measured and calculated bicarbonate values. Clin Chem. 2008;54:1586–7. [PubMed]


text:
There are several AAU basketball teams in Texas that receive periodic national recognition by recruiting analysts. Teams such as the Houston Defenders, Texas Assault, Texas PRO and Houston Hoops get the ink and definitely deserve all the press.
There's a team representing the greater San Antonio area that feels it's every bit as good as the aforementioned -- and it proved it on Tuesday. The Texas D-1 Ambassadors-San Antonio have put together an impressive summer run and have beaten some of the best teams in and out of the state.
Tuesday evening, their beliefs became reality against one traditional Texas power in the finals of the Las Vegas Live Tournament. In an all-Texas clash, the Ambassadors defeated the Hoops, 65-53, to claim the 17U Platinum Bracket championship.
As much as the Ambassadors have won this year (the team is 50-9 this summer entering this weekend's tournament play in California), few victories earned the respect that the win against the Hoops earned. Some even classified the win as a minor upset.
"We obviously have a lot of respect for that group," Ambassadors coach Paul Josephs said, "but our kids came ready to play. They were excited about the opportunity. Our kids feel after everyone we've played, we can compete with anybody."
D-1 Ambassadors founder Max Ivany added: "It's always satisfying to win a major championship. Going into the tournament, Mr. Joseph felt good about the team, and so did I. We felt that had a real honest shot of winning the event. Of course, you need a little luck, and we got that, too."
The Ambassadors have played several of the best teams tough all year, including the Texas Assault, which won the adidas Super 64, also played in Vegas. The Ambassadors won eight consecutive games, the last against highly ranked Division I guards in L.J. Rose and Duke-bound Rasheed Sulaimon. J-Mychal Reese, another star guard for the Hoops, was out with an injury.
The Ambassadors were led by 6-foot-9 Connor Lammert who had several offers entering the tournament and picked up two more from Texas and Stanford during the tournament. He helped the team to an undefeated run through pool and then to bracket-play wins against California-based Greenline Basketball, Nevada-based Marcus Banks Hard 2 Guard, FOH Seattle and the Louisiana Future before meeting the Hoops in the championship game.
While Lammert had a solid tournament, it was the play of his teammates that helped pick up major victories. The backcourt duo of Matt Gramling and Adam Perez ran the offense, while fellow guards Nikko Maxwell and Carter Josephs kept the pace at an even keel. Uche Ofoegbu and Aaron Ramirez were do-it-all swingmen, and Jeff Rodewald and Shelby Lane teamed with Lammert to be the team's interior muscle.
"One of the reasons why I think we're a very good team is because everybody puts team over self," Paul Josephs said. "If Connor tries to do it himself, he may be somewhat successful, but if we let the game dictate who scores, you're going to win your fair share. It was truly a team effort out there."
There is no rest for the new Las Vegas Live champions, as the Ambassadors will compete in the GBOA Challenge of Champions Thursday in Long Beach, Calif.
2013 D-1 Ambassadors team wins Silver Bracket
The San Antonio group wasn't the only Ambassadors team that took home hardware from Vegas.
The Texas D-1 Ambassadors 2013-Bostic defeated the Oklahoma Attack to win the tournament's 17U Silver Bracket. After a 1-2 record in pool play, the guard-oriented Ambassadors, coached by Reginald Bostic, defeated the Oklahoma Shock-Lloyd, Team Missouri and the San Antonio Hurricanes to advance to the bracket finals.
With the assistance and perseverance of players like Justin Moss, Napoleon Onyeje and Rasmus Bach, the Ambassadors took home a 17U title -- despite being a 16U team. Adding to the program's success is the Texas D-1 Ambassadors 2013-Morse, a team that won its pool before bowing out to eventual tournament quarterfinalist DJH5-Houston.
"Honestly, I'd be lying to say it's not gratifying," Ivany said of watching two of his teams win titles. "You get happy because you know the kids are wonderful kids. The San Antonio kids tend not to get the respect as the other teams. As for our 16-and-under teams [D-1 Bostic and D-1 Morse], we expected them both to compete hard and maybe steal a win or two against the 17s. We figured next year would be their year, but they really did some growing on the spot. It was really fun to watch."


text:
pocahontex wrote:...it will make a long name. Sometimes you'll face a difficulty to write your name onto a test paper because there is not enough room to write such a long name.
That's not a big deal my friend. Just write your short name instead of the full one. Take a look at this :mamuta wrote:I haven't thought about it but you're absolutely right!
Hi, my name is pocahontex blablabla blablabla blablabla...
Hallo, my name is mamuta blablabla blablabla blablabla...
Cool huh !!!
Sorry just kidding my friends.
My dear friends, to me, it's not a big deal whether you take your father's name or your mom's name or even both.
But to me, the best one is when you take none of them. Just your name without anything behind or in the front.
Nowadays, lots of people are using their family name to get advantage of the situation. For instance, if his/her father/mother is a public figure or popular artist, they use that name for their interest. Some people are hiding behind their big family name. To me, it's not a proper strategy to use family name to get something.
I wish we didn't have any family name or surneme so that everybody would be equal in any sectors.
Sometimes I'm confused when calling some people who take their parent's name . This is one example.
A grand father has two sons.
Suppose the first one is Marco Ginting and the second one is Marlon Ginting. "Ginting" is the family name.
Both sons are called "Ginting".
When they are in a family gathering, then we call "Ginting". You already know the result right!
The three men would look at you because their names are "Ginting". Can you imagine if there are ten "Gintings" there. What would happen? What a confusing thing huh !!! What a mess!!! :P


text:
Monster Cable 400dfo
Crutchfield Customer Review (What's this?)
Great Fiber Optic Cable. Excellent Build Quality. Solid Terminations on each end.
Pros: High Quality. Good Value.
Cons: None.
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With most stereo and speaker purchases, we offer installation guides, dash kits, wiring harnesses, and speaker accessories at deep discounts. Also, you can just buy our installation guides for $10. (If you buy a new stereo or speakers from us within 60 days, we'll apply the $10 to your order.)Learn more
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Our experts help you pick the ideal gear for your needs.Meet our advisors
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Item # 119DF4001M | MFR # 127612-00
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Shop all Digital Optical Cables
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Since an optical cable carries signals as pulses of light rather than as a stream of electrons, it is virtually impervious to magnetic or electrical interference.
Great Fiber Optic Cable. Excellent Build Quality. Solid Terminations on each end.
Chris B., Valencia, California
Average Customer Review(s):
Great Fiber Optic Cable. Excellent Build Quality. Solid Terminations on each end.
Pros: High Quality. Good Value.
Cons: None.
Big step up from the cable provided with the unit we purchased. Superior quality, durability, sound quality are evident.
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Pros: didn't work for my application
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As usual, good quality from Monster. Crutchfield advisor was very helpful finding and recommending what I needed. Product arrived VERY quickly. The only complaint is the cable doesn't fit the sockets securely and sometimes must be pushed back in to function properly. It's used to connect a T.V. to a soundbar, so the components may be the problem, not the cable . This is the only reason it didn't get five stars. Crutchfield help and service, five stars!
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High end cable!
PERFECT, from the Crutchfield guys to the shipping company. Thank You.
It's hard (almost impossible) to find anything to complain about in the quality of a Monster Cable product, and their TOSLink optical digital audio cable upholds that reputation nicely. Very well made, and produces excellent sound, as a digital transfer cable should. Realistically, there are going to be much -much- cheaper products that will produce the same sound - hey - that's the point of digital loss-less transfer, right? So, you should acknowledge that this is a bit of a vanity purchase. Having said that, it is totally hassle-free, with good-fitting connectors, and it -looks expensive- too. These facts make this cable worth its price only if it is to be used on your high-end equipment where you are striving for not only the best sound, but to show everyone that admires your system that you have made every effort to achieve the finest quality in equipment as well as sound. If you are just going to hook these up where they'll be invisible, you may be spending extra money unnecessarily
Pros: You won't achieve better sound from any other optical digital audio cable and their quality means they will be hassle-free to install, and beautiful to look at.
Cons: They are awfully expensive and there are cheaper alternatives that will be functionally equivalent. This cost them one star in the review. Functionally, they're five star all the way
Monster made all the difference in the world. It made great Polk sound system Much better. I would say if you want great sound get a Monster.pl
Pros: Supper sound improvement , only way to go if you want to really enjoy our sound system
Cons: Kind of expensive, but worth every bit of it.
I have been using Monster Cable products now for 15+ years and I have yet to find any of their analog or digital cables that have failed. Even under any sort of application (home or vehicle audio) or abuse. GREAT PRODUCT!!
Excellent quality.
Sold as compatible with Nuforce headphone AMP. Will not fit
Good cable at a hard to find length (4 meters). I bought this cable for my Gaming system, so the length was perfect for it. And of course you get quality construction that comes with all Monster cables. I would like to have seen the HexMesh-Protective Jacket around the cable like most of my Monster cables have but a good cable none the less.
great product ,great sound
My older receiver lacks DVI inputs so I opted for the optical input. Everything works just fine. I like the construction of Monster Cables and usually use them over cheaper products.
Overview: The Monster 400DFO Digital Optical Cable features specially tuned fiber and precision polished fiber terminations to minimize internal reflections and signal dispersion for more accurate signal transfer and smooth, natural sound. An advanced InsuLight jacket further minimizes digital jitter and time distortion. And because the bitstream is transferred optically, there are no annoying buzzes and hums, just great digital sound.
InsuLight Jacket: InsuLight inner jacket reduces digital jitter and time distortion for more accurate audio reproduction.
Specially Tuned Optical Fiber: Specially tuned optical fiber for low dispersion and higher fidelity.
Polished Fiber Terminations: Precision-polished fiber terminations minimize internal reflections for improved digital signal transfer.
Heavy Duty Molded Connectors: For long-lasting durability and performance.
Heavy-Duty Strain Relief: Heavy-duty strain relief prevents fiber and connector damage during cable installation or removal.
Rubber Grip Connector: O ring rubber grip allows easy connector handling.
Duraflex Protective Jacket: Flexible for easy routing and installation. Resistant to abrasions and temperature extremes.
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