New International Version For the life of a creature is in the blood, and I have given it to you to make atonement for yourselves on the altar; it is the blood that makes atonement for one's life. New Living Translation for the life of the body is in its blood. I have given you the blood on the altar to purify you, making you right with the LORD.
It is the blood, given in exchange for a life, that makes purification possible. English Standard Version For the life of the flesh is in the blood, and I have given it for you on the altar to make atonement for your souls, for it is the blood that makes atonement by the life. Berean Study Bible For the life of the flesh is in the blood, and I have given it to you to make atonement for your souls upon the altar; for it is the blood that makes atonement for the soul. New American Standard Bible 'For the life of the flesh is in the blood, and I have given it to you on the altar to make atonement for your souls; for it is the blood by reason of the life that makes atonement.
Christian Standard Bible For the life of a creature is in the blood, and I have appointed it to you to make atonement on the altar for your lives, since it is the lifeblood that makes atonement. Contemporary English Version Life is in the blood, and I have given you the blood of animals to sacrifice in place of your own. Good News Translation The life of every living thing is in the blood, and that is why the LORD has commanded that all blood be poured out on the altar to take away the people's sins. Blood, which is life, takes away sins. Holman Christian Standard Bible For the life of a creature is in the blood, and I have appointed it to you to make atonement on the altar for your lives, since it is the lifeblood that makes atonement.
International Standard Version because the life of the flesh is in the blood itself, and I myself have given it to you all so that atonement may be made for your souls on the altar, since the blood itself makes atonement through the life that is in it. NET Bible for the life of every living thing is in the blood. Probing fetal development starts, naturally enough, with DNA, the recipe for life. Developmental biologists have already gathered a trove of information here, through studies of laboratory animals from worms to mice, identifying many genes and processes that have human equivalents.
Painstaking detective work on families with inherited genetic diseases has yielded even more insight. Scientists hope to attract millions to 'DNA. But the advent of next-generation DNA sequencing is transforming the field. It is now relatively easy to sequence genomes, in whole or in part, to look for the causes of rare genetic disorders.
And discoveries are piling up: how key signalling proteins help cells to adopt their myriad identities, and how the packaging of DNA influences brain development, to name just two. Most studies so far have parsed genomes after birth. But researchers are pushing to use the same methods on fetuses in the womb, in the hope of improving the diagnoses and prognoses they can offer to expectant parents.
Hurles and his colleagues, for example, are studying 1, fetuses with structural abnormalities spotted through ultrasounds. Researchers want to go still further, and sequence entire fetal genomes using blood from the mother. This would give them ready access to DNA at nearly all stages of fetal development, in healthy fetuses as well as ones that may have problems. The approach is realistic, they say.
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The field is racing ahead: a flurry of papers, from Lo 2 , 3 , Stephen Quake at Stanford University in California 4 , 5 and genome scientist Jay Shendure at the University of Washington in Seattle 6 have honed the resolution with which scientists can analyse a fetal genome from tiny bits of DNA floating in the mother's blood. They can now count the number of chromosomes in a fetus 2 , 4 , and are developing ever-more-accurate ways to sequence genomes.
In principle, they can now detect single-letter variants in the DNA sequence that might cause inherited diseases, and are building up their ability to find mutations that underlie some developmental disorders but are not present in either parent. Several companies have been formed to develop the technologies. There are barriers to overcome before the newest technologies will see widespread use in lab or clinic.
One is the cost. Whole-genome sequencing is getting cheaper, but researchers often need to repeat it many times to boost the resolution of their results 7. But researchers are confident that these roadblocks won't remain. The flip side of personal genomics: When a mutation doesn't spell disease. Interpreting the results will be another sticking point.
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Not all DNA changes cause disorders. And even if an individual carries a specific mutation, scientists cannot yet be sure that it will always result in disease. But as costs drop, scientists say, they will be able to sequence enough genomes to learn which mutations predict disorders with high probability. They then hope to see non-invasive whole-genome sequencing applied as a screening tool during pregnancy. And even before birth might be an option.
A team of scientists is already using next-generation sequencing of specific genes to diagnose brittle-bone disease in fetuses as part of a clinical trial that uses stem cells to treat the condition in the womb. The researchers are currently obtaining the fetal cells through invasive sampling techniques, but aim to switch to non-invasive testing. DNA is but the start of the story of human development.
Researchers are keen to understand how instructions in the genome are deployed in time and space as a fetus grows, and how this goes wrong during disease. Many are therefore focusing on the molecule RNA, which the cell uses to copy — and then act on — a given set of DNA instructions. And that presents fresh challenges. RNA breaks down very quickly, so it is harder to work with than DNA, especially when trying to untangle a fetus's output of RNA — its transcriptome — from the mother's.
To simplify things, clinician and geneticist Diana Bianchi, now director of the National Institute of Child Health and Human Development in Bethesda, Maryland, began by studying the transcriptome of amniotic fluid, which contains freely floating RNA from fetus and placenta. Over the past decade, her team has built up intriguing snapshots of gene activity through the second and third trimesters from discarded samples taken during amniocentesis tests , and at term from samples gleaned during Caesarean sections , as well as some work with maternal blood, which bears free-floating RNA fragments from fetus, mother and placenta.
She has shown how a full-term fetus switches on just the sorts of genes that might be expected for a baby gearing up to be born — including ones involved in lung and gut physiology, energy metabolism, the immune system and the eye 8. Much of Bianchi's work has focused on amniotic-fluid samples from fetuses affected by chromosomal abnormalities, such as Down's syndrome an extra chromosome 21 and Edward's syndrome an extra chromosome She finds that gene activity is abnormal across the whole genome, not just on the extra chromosome, and even in genes needed for brain development 9.
She's also found that cells of fetuses with Down's incur damage from the by-products of metabolism, a condition known as oxidative stress Pregnancy: Prepare for unexpected prenatal test results. This raises the provocative possibility of treating fetuses in the womb to ameliorate the cognitive impairment associated with Down's.
To explore this, Bianchi's team compared transcriptome data from fetuses with and without Down's, and mouse models of the syndrome, to pinpoint patterns associated with the condition Then they scoured a database for molecules that might reverse some of the abnormal patterns, including some drugs that are already approved for human use. Erythrocytes are biconcave disks; that is, they are plump at their periphery and very thin in the center Figure 2. Since they lack most organelles, there is more interior space for the presence of the hemoglobin molecules that, as you will see shortly, transport gases.
The biconcave shape also provides a greater surface area across which gas exchange can occur, relative to its volume; a sphere of a similar diameter would have a lower surface area-to-volume ratio. In the capillaries, the oxygen carried by the erythrocytes can diffuse into the plasma and then through the capillary walls to reach the cells, whereas some of the carbon dioxide produced by the cells as a waste product diffuses into the capillaries to be picked up by the erythrocytes.
Capillary beds are extremely narrow, slowing the passage of the erythrocytes and providing an extended opportunity for gas exchange to occur. However, the space within capillaries can be so minute that, despite their own small size, erythrocytes may have to fold in on themselves if they are to make their way through.
Fortunately, their structural proteins like spectrin are flexible, allowing them to bend over themselves to a surprising degree, then spring back again when they enter a wider vessel. Hemoglobin is a large molecule made up of proteins and iron. It consists of four folded chains of a protein called globin , designated alpha 1 and 2, and beta 1 and 2 Figure 3 a.
Each iron ion in the heme can bind to one oxygen molecule; therefore, each hemoglobin molecule can transport four oxygen molecules. An individual erythrocyte may contain about million hemoglobin molecules, and therefore can bind to and transport up to 1. In the lungs, hemoglobin picks up oxygen, which binds to the iron ions, forming oxyhemoglobin. The bright red, oxygenated hemoglobin travels to the body tissues, where it releases some of the oxygen molecules, becoming darker red deoxyhemoglobin , sometimes referred to as reduced hemoglobin.
Oxygen release depends on the need for oxygen in the surrounding tissues, so hemoglobin rarely if ever leaves all of its oxygen behind. In the capillaries, carbon dioxide enters the bloodstream. About 76 percent dissolves in the plasma, some of it remaining as dissolved CO 2 , and the remainder forming bicarbonate ion. About 23—24 percent of it binds to the amino acids in hemoglobin, forming a molecule known as carbaminohemoglobin.
From the capillaries, the hemoglobin carries carbon dioxide back to the lungs, where it releases it for exchange of oxygen. Ineffective hematopoiesis results in insufficient numbers of RBCs and results in one of several forms of anemia. An overproduction of RBCs produces a condition called polycythemia.
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The primary drawback with polycythemia is not a failure to directly deliver enough oxygen to the tissues, but rather the increased viscosity of the blood, which makes it more difficult for the heart to circulate the blood. In patients with insufficient hemoglobin, the tissues may not receive sufficient oxygen, resulting in another form of anemia.
The device works by sending two different wavelengths of light one red, the other infrared through the finger and measuring the light with a photodetector as it exits. Hemoglobin absorbs light differentially depending upon its saturation with oxygen. The machine calibrates the amount of light received by the photodetector against the amount absorbed by the partially oxygenated hemoglobin and presents the data as percent saturation. Normal pulse oximeter readings range from 95— percent. Lower percentages reflect hypoxemia , or low blood oxygen.
The term hypoxia is more generic and simply refers to low oxygen levels. Oxygen levels are also directly monitored from free oxygen in the plasma typically following an arterial stick. When this method is applied, the amount of oxygen present is expressed in terms of partial pressure of oxygen or simply pO 2 and is typically recorded in units of millimeters of mercury, mm Hg.
In response to hypoxemia, less oxygen will exit the vessels supplying the kidney, resulting in hypoxia low oxygen concentration in the tissue fluid of the kidney where oxygen concentration is actually monitored. Interstitial fibroblasts within the kidney secrete EPO, thereby increasing erythrocyte production and restoring oxygen levels. In a classic negative-feedback loop, as oxygen saturation rises, EPO secretion falls, and vice versa, thereby maintaining homeostasis.
Populations dwelling at high elevations, with inherently lower levels of oxygen in the atmosphere, naturally maintain a hematocrit higher than people living at sea level. Consequently, people traveling to high elevations may experience symptoms of hypoxemia, such as fatigue, headache, and shortness of breath, for a few days after their arrival.
In response to the hypoxemia, the kidneys secrete EPO to step up the production of erythrocytes until homeostasis is achieved once again. To avoid the symptoms of hypoxemia, or altitude sickness, mountain climbers typically rest for several days to a week or more at a series of camps situated at increasing elevations to allow EPO levels and, consequently, erythrocyte counts to rise.
When climbing the tallest peaks, such as Mt. Everest and K2 in the Himalayas, many mountain climbers rely upon bottled oxygen as they near the summit.