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                <text>Clinical death is the medical term for cessation of blood circulation and breathing, the two necessary criteria to sustain human and many other organisms' lives. It occurs when the heart stops beating in a regular rhythm, a condition called cardiac arrest. The term is also sometimes used in resuscitation research.&#13;
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Stopped blood circulation has historically proven irreversible in most cases. Prior to the invention of cardiopulmonary resuscitation (CPR), defibrillation, epinephrine injection, and other treatments in the 20th century, the absence of blood circulation (and vital functions related to blood circulation) was historically considered the official definition of death. With the advent of these strategies, cardiac arrest came to be called clinical death rather than simply death, to reflect the possibility of post-arrest resuscitation.&#13;
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At the onset of clinical death, consciousness is lost within several seconds. Measurable brain activity stops within 20 to 40 seconds. Irregular gasping may occur during this early time period, and is sometimes mistaken by rescuers as a sign that CPR is not necessary. During clinical death, all tissues and organs in the body steadily accumulate a type of injury called ischemic injury.&#13;
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Most tissues and organs of the body can survive clinical death for considerable periods. Blood circulation can be stopped in the entire body below the heart for at least 30 minutes, with injury to the spinal cord being a limiting factor. Detached limbs may be successfully reattached after 6 hours of no blood circulation at warm temperatures. Bone, tendon, and skin can survive as long as 8 to 12 hours.&#13;
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The brain, however, appears to accumulate ischemic injury faster than any other organ. Without special treatment after circulation is restarted, full recovery of the brain after more than 3 minutes of clinical death at normal body temperature is rare. Usually brain damage or later brain death results after longer intervals of clinical death even if the heart is restarted and blood circulation is successfully restored. Brain injury is therefore the chief limiting factor for recovery from clinical death.&#13;
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Although loss of function is almost immediate, there is no specific duration of clinical death at which the non-functioning brain clearly dies. The most vulnerable cells in the brain, CA1 neurons of the hippocampus, are fatally injured by as little as 10 minutes without oxygen. However, the injured cells do not actually die until hours after resuscitation. This delayed death can be prevented in vitro by a simple drug treatment even after 20 minutes without oxygen. In other areas of the brain, viable human neurons have been recovered and grown in culture hours after clinical death. Brain failure after clinical death is now known to be due to a complex series of processes called reperfusion injury that occur after blood circulation has been restored, especially processes that interfere with blood circulation during the recovery period. Control of these processes is the subject of ongoing research.&#13;
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In 1990, the laboratory of resuscitation pioneer Peter Safar discovered that reducing body temperature by three degrees Celsius after restarting blood circulation could double the time window of recovery from clinical death without brain damage from 5 minutes to 10 minutes. This induced hypothermia technique is beginning to be used in emergency medicine. The combination of mildly reducing body temperature, reducing blood cell concentration, and increasing blood pressure after resuscitation was found especially effective—allowing for recovery of dogs after 12 minutes of clinical death at normal body temperature with practically no brain injury. The addition of a drug treatment protocol has been reported to allow recovery of dogs after 16 minutes of clinical death at normal body temperature with no lasting brain injury. Cooling treatment alone has permitted recovery after 17 minutes of clinical death at normal temperature, but with brain injury.&#13;
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Under laboratory conditions at normal body temperature, the longest period of clinical death of a cat (after complete circulatory arrest) survived with eventual return of brain function is one hour.....&#13;
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&#13;
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                <text>The book contains the substance of the lectures and partly of the practices of the subject of ‘Genetics and Genomics’ held in Semmelweis University for medical, pharmacological and dental students. The book does not contain basic genetics and molecular biology, but rather topics from human genetics mainly from medical point of views. Some of the 15 chapters deal with medical genetics, but the chapters also introduce to the basic knowledge of cell division, cytogenetics, epigenetics, developmental genetics, stem cell&#13;
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                <text> The present thesis deals with a deep analysis of the genetic structure of extant human worldwide populations, with a special focus on the Mediterranean. Different genetic markers, 18 Alu insertions and 367 single nucleotide polymorphisms (SNPs), were analysed for the first time in general populations and Bedouins from Jordan. The same SNPs were also genotyped in a consistent set of samples from the Mediterranean Basin. Specifically, Alu markers were used to assess the genetic diversity within Jordan and to define the relationships across present-day Middle Eastern, North African, and European populations. While SNPs located in the top coronary artery disease (CAD) risk regions (1p13, 1q41, 9p21, and 10q11) were used to explore the genetic variation and the LD patterns across 19 populations from Europe, Middle East and North Africa, together with Asian and African samples from the 1000 Genomes Project. Furthermore, Tunisian and Moroccan case-control samples were used to test for the first time the applicability of European GWAS results in these four genomic regions to North African populations. Finally, simulated genomic data were used to evaluate the consistency of association results across European, Asian and Sub-Saharan African case-control samples. Neutral and CAD risk markers pointed out a low but significant geographic structure in the Mediterranean area. As a particular case in the Mediterranean context, Bedouins and general population from Jordan showed statistical differences (p=0.038). The genetic heterogeneity detected is likely related to the fact that urban areas have been subject to several external influences but Bedouins have preserved their own genetic background because of their nomadic and isolated lifestyle. The general patterns of genetic variation observed in the four CAD risk regions analysed are in agreement with the genetic structure generated by demographic processes. Despite this fact, the present work also identified potential signals of positive and balancing selection in some specific risk markers and haplotypes. Actually, potential signatures of positive selection in the 9p21 region and of balancing selection in 9p21 and 10q11 have been observed. The regions under positive or balancing selection are shared across continents but the specific markers under selection are, in some cases, continent-specific. Results from the association study in North Africa revealed significant association signals in the four genomic regions analysed in Moroccan and Tunisian samples confirming the trans-ethnic importance of these genomic regions for the risk of CAD. However, in the meta-analyses performed with the North African case-control samples, only the 9p21 and 10q11 regions showed association signals and none of the North African risk SNPs was associated with CAD in Europe. These arguments suggest the existence of continent-specific CAD risk variants in these chromosomal regions. Significant differences in the LD and in the haplotype patterns confirm the heterogeneity in the genomic structure between North Africans and Europeans. In addition, differences in the LD structure persist even across Europeans, North Africans, Asians, and Sub-Saharan Africans. Finally, the simulation study highlighted an overall consistency in effect direction across populations of different ancestry, specially between Europeans and Asians. Because simulations assumed no actual differences in genetic effect size between populations and because the rate of between-population effect size differences generated by our study was considerably lower than the rate reported from empirical studies using real data, our study supports the existence of real differences in the genetic risk architecture of complex traits between populations. In general, this study confirmed that a substantial fraction of association signals are shared across people of different ancestries. However, some discrepancies in the effect size across populations highlighted the importance of accounting for population structure in association studies.</text>
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