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Rh blood group system
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"Rh-" redirects here. For the Siddharta album, see Rh- (album). For the band, see The RH Factor.
The Rh blood group system (including the Rh factor) is one of thirty-five known human blood group systems. It is the second most important blood group system, after the ABO blood group system. The Rh blood group system consists of 50 defined blood group antigens, among which the five antigens D, C, c, E, and e are the most important. The commonly used terms Rh factor, Rh positive and Rh negative refer to the D antigen only. Besides its role in blood transfusion, the D antigen is used to determine the risk of hemolytic disease of the newborn (or erythroblastosis fetalis) for Rh disease management.
Rh derives from rhesus and the terms rhesus blood group system, rhesus factor, rhesus positive and rhesus negative are also used.
Contents
[hide]
1 Rh factor
2 History of discoveries
3 Rh nomenclature
4 Rh system antigens
5 Hemolytic disease of the newborn
6 Population data
7 Inheritance
8 Function
9 Origin of RHD polymorphism
10 Weak D
11 Partial D
12 Rhnull phenotype
13 Other Rh group antigens
14 Rh antibodies
15 Erythroblastosis Fetalis
16 References
17 External links
Rh factor[edit]
An individual either has, or does not have, the "Rh factor" on the surface of their red blood cells. This term strictly refers only to the most immunogenic D antigen of the Rh blood group system, or the Rh− blood group system. The status is usually indicated by Rh positive (Rh+ does have the D antigen) or Rh negative (Rh− does not have the D antigen) suffix to the ABO blood type. However, other antigens of this blood group system are also clinically relevant. These antigens are listed separately (see below: Rh nomenclature). In contrast to the ABO blood group, immunization against Rh can generally only occur through blood transfusion or placental exposure during pregnancy in women.
History of discoveries[edit]
The rhesus blood type named after the rhesus monkey was first discovered in 1937 by Karl Landsteiner and Alexander S. Wiener. The significance of the discovery was not immediately apparent and was only realized in 1940, after subsequent findings by Philip Levine and Rufus Stetson.[1] This serum that led to the discovery was produced by immunizing rabbits with red blood cells from a rhesus macaque. The antigen that induced this immunization was designated by them as Rh factor to indicate that rhesus blood had been used for the production of the serum.[2]
In 1939, Phillip Levine and Rufus Stetson published in a first case report the clinical consequences of non-recognized Rh factor, hemolytic transfusion reaction and hemolytic disease of the newborn in its most severe form.[3] It was recognized that the serum of the reported woman agglutinated with red blood cells of about 80% of the people although the then known blood groups, in particular ABO were matched. No name was given to this agglutinin when described. In 1940, Karl Landsteiner and Alexander S. Wiener made the connection to their earlier discovery, reporting a serum that also reacted with about 85% of different human red blood cells.[4]
Based on the serologic similarities Rh factor was later also used for antigens, and anti-Rh for antibodies, found in humans such as the previously described by Levine and Stetson. Although differences between these two sera were shown already in 1942 and clearly demonstrated in 1963, the already widely used term "Rh" was kept for the clinically described human antibodies which are different from the ones related to the rhesus monkey. This real factor found in rhesus macaque was classified in the Landsteiner-Wiener antigen system (antigen LW, antibody anti-LW) in honor of the discoverers. [5][6]
It was recognized that the Rh factor was just one in a system of various antigens. Based on different models of genetic inheritance, two different terminologies were developed; both of them are still in use.
The clinical significance of this highly immunizing D antigen (i.e. Rh factor) was soon realized. Some keystones were to recognize its importance for blood transfusion (including reliable diagnostic tests), hemolytic disease of the newborn (including exchange transfusion), and very importantly the prevention of it by screening and prophylaxis.
The discovery of fetal cell-free DNA in maternal circulation by Holzgrieve et al. led to the noninvasive genotyping of fetal Rh genes in many countries.
Rh nomenclature[edit]
Rh haplotype notation
Fisher-Race
Wiener
Dce R0
DCe R1
DcE R2
DCE RZ
dce r
dCe r′
dcE r″
dCE rY
The Rh blood group system has two sets of nomenclatures: one developed by Ronald Fisher and R.R. Race, the other by Wiener. Both systems reflected alternative theories of inheritance. The Fisher-Race system, which is more commonly in use today, uses the CDE nomenclature. This system was based on the theory that a separate gene controls the product of each corresponding antigen (e.g., a "D gene" produces D antigen, and so on). However, the d gene was hypothetical, not actual.
The Wiener system used the Rh–Hr nomenclature. This system was based on the theory that there was one gene at a single locus on each chromosome, each contributing to production of multiple antigens. In this theory, a gene R1 is supposed to give rise to the “blood factors” Rh0, rh′, and rh″ (corresponding to modern nomenclature of the D, C and E antigens) and the gene r to produce hr′ and hr″ (corresponding to modern nomenclature of the c and e antigens).[7]
Notations of the two theories are used interchangeably in blood banking (e.g., Rho(D) meaning RhD positive). Wiener’s notation is more complex and cumbersome for routine use. Because it is simpler to explain, the Fisher-Race theory has become more widely used.
DNA testing has shown that both are partially correct.[citation needed] There are in fact two linked genes, the RHD gene which produces a single immune specificity (anti-D) and the RHCE gene with multiple specificities (anti-C, anti-c, anti-E, anti-e). Thus, Wiener’s postulate that a gene could have multiple specificities (something many did not give credence to originally) has been proven correct. On the other hand, Wiener’s theory that there is only one gene has proven incorrect, as has the Fischer-Race theory that there are three genes, rather than the 2. The CDE notation used in the Fisher-Race nomenclature is sometimes rearranged to DCE to more accurately represent the co-location of the C and E encoding on the RhCE gene, and to make interpretation easier.
Rh system antigens[edit]
The proteins which carry the Rh antigens are transmembrane proteins, whose structure suggest that they are ion channels.[8] The main antigens are D, C, E, c and e, which are encoded by two adjacent gene loci, the RHD gene which encodes the RhD protein with the D antigen (and variants)[9] and the RHCE gene which encodes the RhCE protein with the C, E, c and e antigens (and variants).[10] There is no d antigen. Lowercase "d" indicates the absence of the D antigen (the gene is usually deleted or otherwise nonfunctional).
Rh phenotypes are readily identified by identifying the presence or absence of the Rh surface antigens. As can be seen in the table below, most of the Rh phenotypes can be produced by several different Rh genotypes. The exact genotype of any individual can only be identified by DNA analysis. Regarding patient treatment, only the phenotype is usually of any clinical significance to ensure a patient is not exposed to an antigen they are likely to develop antibodies against. A probable genotype may be speculated on, based on the statistical distributions of genotypes in the patient’s place of origin.
R0 (cDe) is today most common in Africa. The allele was thus often assumed in early blood group analyses to have been typical of populations on the continent; particularly in areas below the Sahara. Given the presence of high R0 percentages among Sephardim and Ashkenazim Jews compared to native European populations and the relative genetic isolation of Ashkenazim, Ottensooser et al. (1963) therefore suggested that high R0 frequencies were likely characteristic of the ancient Palestine Jews, who had emigrated from Egypt prior to their dispersal throughout the Mediterranean Basin and Europe.[11] However, more recent studies have found R0 frequencies as low as 24.3% among some Afroasiatic-speaking groups in the Horn of Africa,[12] as well as higher R0 frequencies among certain other Afroasiatic speakers in North Africa (37.3%)[13] and among some Palestinians in the Levant (30.4%).[14]
Rh phenotypes and genotypes
Phenotype expressed on cell
Genotype expressed in DNA
Prevalence
(%) †
Fisher-Race notation
Wiener notation
D+ C+ E+ c+ e+ (RhD+) Dce/DCE R0RZ 0.0125
Dce/dCE R0rY 0.0003
DCe/DcE R1R2 11.8648
DCe/dcE R1r″ 0.9992
DcE/dCe R2r′ 0.2775
DCE/dce RZr 0.1893
D+ C+ E+ c+ e− (RhD+) DcE/DCE R2RZ 0.0687
DcE/dCE R2rY 0.0014
DCE/dcE RZr″ 0.0058
D+ C+ E+ c− e+ (RhD+) DCe/dCE R1rY 0.0042
DCE/dCe RZr′ 0.0048
DCe/DCE R1RZ 0.2048
D+ C+ E+ c− e− (RhD+) DCE/DCE RZRZ 0.0006
DCE/dCE RZrY < 0.0001
D+ C+ E− c+ e+ (RhD+) Dce/dCe R0r′ 0.0505
DCe/dce R1r 32.6808
DCe/Dce R1R0 2.1586
D+ C+ E− c− e+ (RhD+) DCe/DCe R1R1 17.6803
DCe/dCe R1r′ 0.8270
D+ C− E+ c+ e+ (RhD+) DcE/Dce R2R0 0.7243
Dce/dcE R0r″ 0.0610
DcE/dce R2r 10.9657
D+ C− E+ c+ e− (RhD+) DcE/DcE R2R2 1.9906
DcE/dcE R2r″ 0.3353
D+ C− E− c+ e+ (RhD+) Dce/Dce R0R0 0.0659
Dce/dce R0r 1.9950
D− C+ E+ c+ e+ (RhD−) dce/dCE rrY 0.0039
dCe/dcE r′r″ 0.0234
D− C+ E+ c+ e− (RhD−) dcE/dCE r″rY 0.0001
D− C+ E+ c− e+ (RhD−) dCe/dCE r′rY 0.0001
D− C+ E+ c− e− (RhD−) dCE/dCE rYrY < 0.0001
D− C+ E− c+ e+ (RhD−) dce/dCe rr′ 0.7644
D− C+ E− c− e+ (RhD−) dCe/dCe r′r′ 0.0097
D− C− E+ c+ e+ (RhD−) dce/dcE rr″ 0.9235
D− C− E+ c+ e− (RhD−) dcE/dcE r″r″ 0.0141
D− C− E− c+ e+ (RhD−) dce/dce rr 15.1020
† Figures taken from a study performed in 1948 on a sample of 2000 people in the United Kingdom.[15]
Rh phenotypes in patients and donors in Turkey[16]
Rh Phenotype
CDE
Patients (%)
Donors (%)
R1r CcDe 37.4 33.0
R1R2 CcDEe 35.7 30.5
R1R1 CDe 5.7 21.8
rr ce 10.3 11.6
R2r cDEe 6.6 10.4
R0R0 cDe 2.8 2.7
R2R2 cDE 2.8 2.4
rr″ cEe – 0.98
RZRZ CDE – 0.03
rr′ Cce 0.8 –
Hemolytic disease of the newborn[edit]
Main article: Hemolytic disease of the newborn
The hemolytic condition occurs when there is an incompatibility between the blood types of the mother and the fetus. There is also potential incompatibility if the mother is Rh negative and the father is positive. When any incompatibility is detected, the mother often receives an injection at 28 weeks gestation and at birth to avoid the development of antibodies toward the fetus. These terms do not indicate which specific antigen-antibody incompatibility is implicated. The disorder in the fetus due to Rh D incompatibility is known as erythroblastosis fetalis.
Hemolytic comes from two words: "hemo" (blood) and "lysis" (destruction) or breaking down of red blood cells
Erythroblastosis refers to the making of immature red blood cells
Fetalis refers to the fetus.
When the condition is caused by the Rh D antigen-antibody incompatibility, it is called Rh D Hemolytic disease of the newborn or Rh disease. Here, sensitization to Rh D antigens (usually by feto-maternal transfusion during pregnancy) may lead to the production of maternal IgG anti-D antibodies which can pass through the placenta. This is of particular importance to D negative females at or below childbearing age, because any subsequent pregnancy may be affected by the Rh D hemolytic disease of the newborn if the baby is D positive. The vast majority of Rh disease is preventable in modern antenatal care by injections of IgG anti-D antibodies (Rho(D) Immune Globulin). The incidence of Rh disease is mathematically related to the frequency of D negative individuals in a population, so Rh disease is rare in old-stock populations of Africa and the eastern half of Asia, and the Indigenous peoples of Oceania and the Americas, but more common in other genetic groups, most especially Western Europeans, but also other West Eurasians, and to a lesser degree, native Siberians, as well as those of mixed-race with a significant or dominant descent from those (e.g. the vast majority of Latin Americans and Central Asians).
Symptoms and signs in the fetus:
Enlarged liver, spleen, or heart and fluid buildup in the fetus' abdomen seen via ultrasound.
Symptoms and signs in the newborn:
Anemia that creates the newborn’s pallor (pale appearance).
Jaundice or yellow discoloration of the newborn’s skin, sclera or mucous membrane. This may be evident right after birth or after 24–48 hours after birth. This is caused by bilirubin (one of the end products of red blood cell destruction).
Enlargement of the newborn’s liver and spleen.
The newborn may have severe edema of the entire body.
Dyspnea or difficulty breathing.
Population data[edit]
The frequency of Rh factor blood types and the RhD neg allele gene differs in various populations.
Population data for the Rh D factor and RhD neg allele[17]
Population
Rh(D) Neg
Rh(D) Pos
Rh(D) Neg alleles
African Americans ∼ 7% 93% ∼ 26%
Asian (Republic of Korea) ∼ 10% > 90% 1%
Basques[18] 21%-36% 65% ∼ 60%
Britain[19] 17% 83%
China[19] <1% <99%
Ethiopians[19] 1%-21% 99%-79%
Europeans (others) 16% 84% 40%
India[19] 0.6%-8.4% 99.4%-91.6%
Indonesia[19] <1% <99%
Japan[19] <1% <99%
Madagascar[19] 1% 99%
Moroccans[19] 29% 71%
Native Americans ∼ 1% 99% ∼ 10%
Saudi Arabia[19] 29% 71%
Subequatorial Africa[19] 1%-3% 99%-97%
United States[19] 15% 85%
Inheritance[edit]
If both of a child’s parents are Rh negative, the child will definitely be Rh negative. Otherwise the child may be Rh positive or Rh negative, depending on the parents' specific genotypes.[20]
The D antigen is inherited as one gene (RHD) (on the short arm of the first chromosome, p36.13–p34.3) with various alleles. Though very much simplified, one can think of alleles that are positive or negative for the D antigen. The gene codes for the RhD protein on the red cell membrane. D− individuals who lack a functional RHD gene do not produce the D antigen, and may be immunized by D+ blood.
The epitopes for the next 4 most common Rh antigens, C, c, E and e are expressed on the highly similar RhCE protein that is genetically encoded in the RHCE gene, also found on chromosome 1. It has been shown that the RHD gene arose by duplication of the RHCE gene during primate evolution.[citation needed] Mice have just one RH gene.[21]
The RHAG gene, responsible for encoding Rh-associated glycoprotein (RhAG) is found on chromosome 6a.
The polypeptides produced from the RHD and RHCE genes form a complex on the red blood cell membrane with the Rh-associated glycoprotein.[22]
Function[edit]
On the basis of structural homology it has been proposed that the product of RHD gene, the RhD protein, is a membrane transport protein of uncertain specificity (CO2 or NH3) and unknown physiological role.[23][24] The three-dimensional structure of the related RHCG protein and biochemical analysis of the RhD protein complex indicates that the RhD protein is one of three subunits of an ammonia transporter.[25][26] Three recent studies[27][28][29] have reported a protective effect of the RhD-positive phenotype, especially RhD heterozygosity, against the negative effect of latent toxoplasmosis on psychomotor performance in infected subjects. RhD-negative compared to RhD-positive subjects without anamnestic titres of anti-Toxoplasma antibodies have shorter reaction times in tests of simple reaction times. And conversely, RhD-negative subjects with anamnestic titres (i.e. with latent toxoplasmosis) exhibited much longer reaction times than their RhD-positive counterparts. The published data suggested that only the protection of RhD-positive heterozygotes was long term in nature; the protection of RhD-positive homozygotes decreased with duration of the infection while the performance of RhD-negative homozygotes decreased immediately after the infection. The overall change in reaction times was always larger in the RhD-negative group than in the RhD-positive.
Origin of RHD polymorphism[edit]
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For a long time, the origin of RHD polymorphism was an evolutionary enigma.[30][31][32] Before the advent of modern medicine, the carriers of the rarer allele (e.g. RhD-negative women in a population of RhD positives or RhD-positive men in a population of RhD negatives) were at a disadvantage as some of their children (RhD-positive children born to preimmunised RhD-negative mothers) were at a higher risk of fetal or newborn death or health impairment from hemolytic disease. It was suggested that higher tolerance of RhD-positive heterozygotes against Toxoplasma-induced impairment of reaction time [27][28] and Toxoplasma-induced increase of risk of traffic accident[29] could counterbalance the disadvantage of the rarer allele and could be responsible both for the initial spread of the RhD allele among the RhD-negative population and for a stable RhD polymorphism in most human populations. It was also suggested that differences in the prevalence of Toxoplasma infection between geographical regions (0–95%) could also explain the striking variation in the frequency of RhD-negative alleles between populations. According to some parasitologists [27] it is possible that the better psychomotor performance of RhD-negative subjects in the Toxoplasma-free population could be the reason for spreading of the “d allele” (deletion) in the European population. In contrast to the situation in Africa and certain (but not all) regions of Asia, the abundance of wild cats (definitive hosts of Toxoplasma gondii) in Europe was very low before the advent of the domestic cat.
Weak D[edit]
In serologic testing, D positive blood is easily identified. Units which are D negative are often retested to rule out a weaker reaction. This was previously referred to as Du, which has been replaced.[33]:322 By definition, weak D phenotype is characterized by negative reaction with anti-D reagent at immediate spin (IS), negative reaction after 37 °C incubation, and positive reaction at anti-human globulin (AHG) phase. Weak D phenotype can occur in several ways. In some cases, this phenotype occurs because of an altered surface protein that is more common in people of European descent. An inheritable form also occurs, as a result of a weakened form of the R0 gene. Weak D may also occur as "C in trans", whereby a C gene is present on the opposite chromosome to a D gene (as in the combination R0r', or "Dce/dCe"). The testing is difficult, since using different anti-D reagents, especially the older polyclonal reagents, may give different results.
The practical implication of this is that people with this sub-phenotype will have a product labeled as "D positive" when donating blood. When receiving blood, they are sometimes typed as a "D negative", though this is the subject of some debate. Most "Weak D" patients can receive "D positive" blood without complications.[33]:323 However, it is important to correctly identify the ones that have to be considered D+ or D−. This is important, since most blood banks have a limited supply of "D negative" blood and the correct transfusion is clinically relevant. In this respect, genotyping of blood groups has much simplified this detection of the various variants in the Rh blood group system.
Partial D[edit]
It is important to differentiate weak D (due to a quantitative difference in the D antigen) from partial D (due to a qualitative difference in the D antigen). Simply put, the weak D phenotype is due to a reduced number of D antigens on a red blood cell. In contrast, the partial D phenotype is due to an alteration in D-epitopes. Thus, in partial D, the number of D antigens is not reduced but the protein structure is altered. These individuals, if alloimmunized to D, can produce an anti-D antibody. Therefore, partial D patients who are donating blood should be labeled as D-positive but, if receiving blood, they should be labeled as D-negative and receive D-negative units.[22]
In the past, partial D was called 'D mosaic' or 'D variant.' Different partial D phenotypes are defined by different D epitopes on the outer surface of the red blood cell membrane. More than 30 different partial D phenotypes have been described.[22]
Rhnull phenotype[edit]
Rhnull individuals have no Rh antigens (no Rh or RhAG) on their red blood cells.[34] This condition is rare.[34] As a consequence of Rh antigen absence, Rhnull red blood cells also lack LW and Fy5 and show weak expression of S, s, and U antigens. Red blood cells lacking Rh/RhAG proteins have structural abnormalities (such as stomatocytosis) and cell membrane defects that can result in hemolytic anemia.[22][34]
Other Rh group antigens[edit]
Currently, 50 antigens have been described in the Rh group system; among those described here, the D, C, c, E and e antigens are the most important. The others are much less frequently encountered or are rarely clinically significant. Each is given a number, though the highest assigned number (CEST or RH57 according to the ISBT terminology) is not an accurate reflection of the antigens encountered since many (e.g. Rh38) have been combined, reassigned to other groups, or otherwise removed.[33]:324
Rh antibodies[edit]
Rh antibodies are IgG antibodies which are acquired through exposure to Rh-positive blood (generally either through pregnancy or transfusion of blood products). The D antigen is the most immunogenic of all the non-ABO antigens. Approximately 80% of individuals who are D-negative and exposed to a single D-positive unit will produce an anti-D antibody. The percentage of alloimmunization is significantly reduced in patients who are actively exsanguinating.[35]
All Rh antibodies except D display dosage (antibody reacts more strongly with red cells homozygous for an antigen than cells heterozygous for the antigen (EE stronger reaction vs Ee).
If anti-E is detected, the presence of anti-c should be strongly suspected (due to combined genetic inheritance). It is therefore common to select c-negative and E-negative blood for transfusion patients who have an anti-E. Anti-c is a common cause of delayed hemolytic transfusion reactions.[22]
Erythroblastosis Fetalis[edit]
Rh agglutinins (antibodies) are capable of causing hemolytic transfusion reactions with extravascular hemolysis. They may also result in severe hemolytic disease of the fetus and newborn (HDFN or HDN) when a Rh negative mother who has had an Rh positive baby before carries an Rh positive fetus, as the Rh agglutinogens from the fetus trigger an immune response from the mother, producing Rh agglutinins and causing the blood of the fetus to agglutinate. Symptoms in the newborn usually include an abnormally large liver or spleen, anemia or low red blood cell count, and in serious cases, swelling of the skin or internal organs.[36] Treatment of the mother with Rh-immunoglobulin (RhIg) during term may help prevent the formation of antibody directed against the D antigen, preventing HDFN in future pregnancies..
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^ Jump up to: a b Flegr J, Novotná M, Lindová J, Havlícek J (2008). "Neurophysiological effect of the Rh factor. Protective role of the RhD molecule against Toxoplasma-induced impairment of reaction times in women" (PDF). Neuroendocrinology Letters. 29 (4): 475–481. PMID 18766148.
^ Jump up to: a b Flegr J, Klose J, Novotná M, Berenreitterová M, Havlícek J (2009). "Increased incidence of traffic accidents in Toxoplasma-infected military drivers and protective effect RhD molecule revealed by a large-scale prospective cohort study.". BMC Infect. Dis. 9: 72. PMC 2692860  . PMID 19470165. doi:10.1186/1471-2334-9-72.
Jump up ^ Haldane JBF (1942). "Selection against heterozygosis in Man.". Eugenics. 11: 333–340. doi:10.1111/j.1469-1809.1941.tb02297.x.
Jump up ^ Fisher RA, Race RR, Taylor GL (1944). "Mutation and the Rhesus reaction". Nature. 153: 106. doi:10.1038/153106b0.
Jump up ^ Li CC (1953). "Is the Rh facing a crossroad? A critique of the compensation effect.". Am Nat. 87: 257–261. doi:10.1086/281782.
^ Jump up to: a b c Brecher ME (2005). Technical Manual (15th ed.). Bethesda MD: American Association of Blood Banks. ISBN 1-56395-196-7.
^ Jump up to: a b c Cartron, J.P. (December 1999). "RH blood group system and molecular basis of Rh-deficiency". Best Practice & Research Clinical Haematology. 12 (4): 655–689. PMID 10895258. doi:10.1053/beha.1999.0047.
Jump up ^ Roback et al. AABB Technical Manual, 16th Ed. Bethesda, AABB Press, 2008.
Jump up ^ "Erythroblastosis Fetalis". Erythroblastosis Fetalis. The Free Dictionary by Farlax. Retrieved 30 May 2015.
External links[edit]
Rh at BGMUT Blood Group Antigen Gene Mutation Database at NCBI, NIH
Article commemorating the first appearance of the Rh factor in the New York Times
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Great Rift Valley
From Wikipedia, the free encyclopedia
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For other uses, see Great Rift Valley (disambiguation).
This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (November 2012) (Learn how and when to remove this template message)
The Great Rift Valley is a continuous geographic trench, approximately 6,000 kilometres (3,700 mi) in length, that runs from Lebanon's Beqaa Valley in Asia to Mozambique in Southeastern Africa.[1] The name continues in some usages, although it is today considered geologically imprecise as it combines features that are today regarded as separate, although related, rift and fault systems.
Today, the term is most often used to refer to the valley of the East African Rift, the divergent plate boundary which extends from the Afar Triple Junction southward across eastern Africa, and is in the process of splitting the African Plate into two new separate plates. Geologists generally refer to these incipient plates as the Nubian Plate and the Somali Plate.
Contents
1 Theoretical extent
2 Asia
3 Africa
4 See also
5 References
6 Further reading
7 External links
Theoretical extent[edit]
Satellite image of a graben in the Afar Depression
Diagram of a rift valley's future evolution into a sea
Map of the Great Rift Valley
The Great Rift Valley as originally described was thought to extend from Lebanon in the north to Mozambique in the south, where it constitutes one of two distinct physiographic provinces of the East African mountains. It included what we would call today the Lebanese section of the Dead Sea Transform, the Jordan Rift Valley, Red Sea Rift and the East African Rift.[2]
Today these rifts and faults are seen as distinct, although connected. These were only formed 35 million years ago.
Asia[edit]
Further information: Sinai Peninsula
The Sinai Peninsula at center and the Dead Sea and Jordan Valley above
The northernmost part of the Rift corresponds to the central section of what is called today the Dead Sea Transform (DST) or Rift. This midsection of the DST forms the Beqaa Valley in Lebanon, separating the Lebanon from the Anti-Lebanon Mountains. Further south it is known as the Hula Valley separating the Galilee mountains and the Golan Heights.[3]
The Jordan River begins here and flows southward through Lake Hula into the Sea of Galilee in Israel. The Rift then continues south through the Jordan Rift Valley into the Dead Sea on the Israeli-Jordanian border. From the Dead Sea southwards, the Rift is occupied by the Wadi Arabah, then the Gulf of Aqaba, and then the Red Sea.[3]
Off the southern tip of Sinai in the Red Sea, the Dead Sea Transform meets the Red Sea Rift which runs the length of the Red Sea. The Red Sea Rift comes ashore to meet the East African Rift and the Aden Ridge in the Afar Depression of East Africa. The junction of these three rifts is called the Afar Triple Junction.[3]
Africa[edit]
Main article: East African Rift
East African Rift Valley
A map of East Africa showing some of the historically active volcanoes (red triangles) and the Afar Triangle (shaded, center)—a triple junction where three plates are pulling away from one another: the Arabian Plate, and the two parts of the African Plate (the Nubian and the Somali) splitting along the East African Rift Zone (USGS).
The East African rift has two branches, the Western Rift Valley and the Eastern Rift Valley.
The Western Rift, also called the Albertine Rift, is bordered by some of the highest mountains in Africa, including the Virunga Mountains, Mitumba Mountains, and Ruwenzori Range. It contains the Rift Valley lakes, which include some of the deepest lakes in the world (up to 1,470 metres (4,820 ft) deep at Lake Tanganyika).
Much of this area lies within the boundaries of national parks such as Virunga National Park in the Democratic Republic of Congo, Rwenzori National Park and Queen Elizabeth National Park in Uganda, and Volcanoes National Park in Rwanda. Lake Victoria is considered to be part of the rift valley system although it actually lies between the two branches. All of the African Great Lakes were formed as the result of the rift, and most lie within its rift valley.
In Kenya, the valley is deepest to the north of Nairobi. As the lakes in the Eastern Rift have no outlet to the sea and tend to be shallow, they have a high mineral content as the evaporation of water leaves the salts behind. For example, Lake Magadi has high concentrations of soda (sodium carbonate) and Lake Elmenteita, Lake Bogoria, and Lake Nakuru are all strongly alkaline, while the freshwater springs supplying Lake Naivasha are essential to support its current biological variety.
The southern section of the Rift Valley includes Lake Malawi, the third-deepest freshwater body in the world, reaching 706 metres (2,316 ft) in depth and separating the Nyassa plateau of Northern Mozambique from Malawi; it ends in the Zambezi valley.
See also[edit]
Great Rift Valley, Ethiopia
The Great Rift: Africa's Wild Heart, a BBC/Animal Planet production
Main earthquakes
1837 Galilee earthquake
2005 Lake Tanganyika earthquake
2008 Lake Kivu earthquake
References[edit]
Jump up ^ Merriam-Webster, Inc 편집부 (1997). MERRIAM WEBSTER'S GEOGRAPHICAL DICTIONARY 3/E(H). Merriam-Webster. p. 444. ISBN 978-0-87779-546-9. Retrieved 22 November 2012.
Jump up ^ Philip Briggs; Brian Blatt (15 July 2009). Ethiopia: the Bradt travel guide. Bradt Travel Guides. p. 450. ISBN 978-1-84162-284-2. Retrieved 22 November 2012.
^ Jump up to: a b c G. Yirgu; C. J. (Cindy J.) Ebinger; P. K. H. Maguire (2006). The Afar Volcanic Province Within the East African Rift System: Special Publication No 259. Geological Society. pp. 306–307. ISBN 978-1-86239-196-3. Retrieved 22 November 2012.
Further reading[edit]
Africa's Great Rift Valley, 2001, ISBN 0-8109-0602-3
Tribes of the Great Rift Valley, 2007, ISBN 978-0-8109-9411-9
East African Rift Valley lakes, 2006, OCLC 76876862
Photographic atlas of the Mid-Atlantic Ridge Rift Valley, 1977, ISBN 0-387-90247-3
Rift Valley fever : an emerging human and animal problem, 1982, ISBN 92-4-170063-7
Rift valley: definition and geologic significance, Giacomo Corti (National Research Council of Italy, Institute of Geosciences and Earth Resources) – The Ethiopian Rift Valley, 2013, [1]
Big crack is evidence that East Africa could be splitting in two, by Lucia Perez Diaz, CNN. Updated April 5, 2018
External links[edit]
Wikimedia Commons has media related to Great Rift Valley.
Article on geology.com
Geological Structure
"Great Rift Valley". New International Encyclopedia. 1905.
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GND: 4520884-0
Retrieved from "https://en.wikipedia.org/w/index.php?title=Great_Rift_Valley&oldid=860304183"
Categories:
Great Rift Valley
Geography of Rift Valley Province
Rifts and grabens
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Saving Face (2004 film)
From Wikipedia, the free encyclopedia
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Saving Face
Saving Face film poster
Directed by
Alice Wu
Produced by
Will Smith
James Lassiter
Teddy Zee
Written by
Alice Wu
Starring
Michelle Krusiec
Joan Chen
Lynn Chen
Music by
Anton Sanko
Cinematography
Harlan Bosmajian
Edited by
Susan Graef
Sabine Hoffmann
Production
company
Destination Films
Distributed by
Sony Pictures Classics
Release date
September 12, 2004 (2004-09-12)
Running time
91 minutes
Country
United States
Language
English
Mandarin
Shanghainese
Saving Face is a 2004 American romantic comedy drama film directed by Alice Wu. The film focuses on Wilhelmina, a young Chinese-American surgeon; her unwed, pregnant mother; and her dancer girlfriend.
The name itself is a reference to the pan-East Asian social concept of face.
Contents
[hide]
1 Plot
2 Cast
3 Background
4 Release
4.1 Box office
4.2 Critical reception
4.3 Awards
5 See also
6 References
7 External links
Plot[edit]
Wilhelmina ("Wil"), a successful young Chinese American surgeon, lives in New York City. Forced by her mother Gao to come to the typical gathering at Planet China amongst family friends, Wil is closeted to her mother and the rest of the older adults. Her mother has plans to set her up with a son of a friend. Wil is drawn to Vivian, the daughter of one of the Chinese mothers who recently got a divorce. They run into each other at the hospital where Wil works, only to discover that Vivian's father is Wil's boss. Vivian and her father have a tense relationship since Vivian is currently pursuing her love of modern dance instead of the more respectable ballet.
Wil comes home to discover her mother has been kicked out by her grandfather for being pregnant out of wedlock, bringing shame to the family. Wil asks for the identity of the father, but Gao refuses to answer. From then on, Gao lives with Wil. Vivian invites Wil to one of her dance shows and after the show, the two hang out. Vivian reveals the fact that they had met once before when they were children; Vivian kissed Wil on the nose after Wil rescued her from bullies; Wil ran away afterwards. Vivian and Wil go to Vivian's apartment and the two kiss.
The couple goes on several dates, but Wil is afraid of kissing Vivian in public. Set up by Wil, Gao goes on several dates to find a man to father her child but remains uninterested. She debates on whether to accept the affections of Cho, a man who has loved her for 15 years and is willing to father the child. On Vivian's request, Wil presents Vivian to her mother as a friend so that they can meet and the three share an awkward dinner. It is revealed later that her mother knows of her homosexuality, but is in denial of it.
Vivian reveals to Wil that she was accepted into a prestigious ballet program in Paris and is considering the offer. Wil congratulates Vivian and gives her encouragement to accept the offer. While Vivian still debates on the offer, Vivian's father speaks to Wil and talks her into convincing Vivian to accept the offer. Wil then breaks up with her, knowing the offer is best for Vivian's career.
Gao accepts Cho's marriage proposal. At the wedding, Wil interrupts with a love note from the father of the child saying how much he loves her and wants to marry her despite their large age gap. Wil points out the elderly pharmacist Yu as the father, who protests. The son of the pharmacist stands up and admits he is the father of the child. Wil and her mother run out of the wedding and onto a bus, laughing. After realizing that love dominates over societal expectations, Wil rushes to the airport to catch Vivian. Wil apologizes, but Vivian challenges Wil to kiss her to prove her sincerity. Unable to publicly display her love out of fear, Wil is left at the terminal as Vivian leaves for Paris.
Three months later, Wil goes to another party at Planet China, and Gao is now a couple with the father of her child. Wil sees Vivian, who has come to see her mother. Wil approaches her and asks her to dance, even though there's no music, and kisses her in front of everyone. Gao and Vivian's mother smile at each other while giving a thumbs up, revealing they planned the reunion, while some people leave in disgust at their behavior. The girls ignore them, while everyone else joins in to dance.
Cast[edit]
Lynn Chen as Vivian Shing
Michelle Krusiec as Wilhelmina Pang
Joan Chen as Hwei-lang Gao (Mother)
Jin Wang as Wai Gung (Grandfather)
Guang Lan Koh as Wai Po (Grandmother)
Jessica Hecht as Randi
Ato Essandoh as Jay
Wang Luoyong as Dr. Shing
David Shih as Norman
Brian Yang as Yu
Nathaniel Geng as Stimson Cho
Mao Zhao as Old Yu
Background[edit]
Alice Wu, who directed the movie, wrote the script several years earlier, drawing on her own experiences "coming out."[1] In 2001, the script won the CAPE screenwriting award, which led to the production of the film. Filming began in fall 2003 on the $2.5 million project.[2]
Featuring the New York City Chinese-American community, the film is in a mixture of Mandarin Chinese and English.
Release[edit]
Saving Face premiered at the Toronto International Film Festival on 12 September 2004, and made its way around the independent film circuit, screening at Sundance Film Festival, Seattle International Film Festival et al.; before going into a very limited release in the US on 27 May 2005.[3]
Box office[edit]
Saving Face initially opened at only 6 theaters, making $75,104 (averaging $12,517/theater) in its opening weekend, and went on to gross $1,187,266 from 56 theaters in its theatrical run.[4] It grossed an additional $49,252 in the UK, for a worldwide gross of $1,236,518.[4]
Critical reception[edit]
The critical reaction to the movie was mostly positive, with most critics praising the tender romance and the light-hearted comedy, although some critics lambasted it for a lack of depth and a "soap opera-like" ending.
Stephen Holden of The New York Times,[5] Wesley Morris of the Boston Globe,[6] Ed Park of Village Voice,[7] among others, gave positive reviews, with Holden in particular calling it an 'amiable' romance spanning three generations of Chinese-Americans.[5] Holden's overall positive review noted that the film had failings at the end: "Sadly, as "Saving Face" ties up the strands of its story, it forfeits its credibility at a wedding finale with a series of instant feel-good solutions and reconciliations."[5]
Jonathan Rosenbaum of the Chicago Reader was notably critical of the film,[8] especially the latter half, describing it as collapsing into "nonsense".[8]
Autostraddle ranked the film #3 of the best 102 Lesbian Movies of All Time.[9]
It currently holds a rating of 87% at Rotten Tomatoes giving making it certified "Fresh",[10] and 65% at Metacritic.[11]
Awards[edit]
Saving Face was nominated for the Breakthrough Director Award at the 2005 Gotham Awards,[12] the Viewer's Choice Award and the Best Actress Award for Michelle Krusiec at the 2005 Golden Horse Film Festival,[12] and the GLAAD Media Award for Outstanding Film in Limited Release at the 2006 GLAAD Media Awards.[12] Out of these, it won the Viewer's Choice Award at the 2005 Golden Horse Film Festival.[12]
See also[edit]
List of LGBT films directed by women
References[edit]
Jump up ^ Johnson, G. Allen (June 6, 2005). "Alice Wu saved up her own doubts and struggles and turned them into the new comedy 'Saving Face'". San Francisco Chronicle.
Jump up ^ Leibowitz, Ed (May 29, 2005). "Kissing Vivian Shing". New York Times. Retrieved 2008-07-06.
Jump up ^ "Saving Face (2004)- Release dates". IMDB. Retrieved 2009-07-17.
^ Jump up to: a b "Saving Face (2005)". Box Office Mojo. Retrieved 2009-07-17.
^ Jump up to: a b c Holden, Stephen (27 May 2005). "Juggling Her Chinese Clan, Gay Lover, Pregnant Mom". The New York Times. Retrieved 17 July 2009.
Jump up ^ Morris, Wesley (10 June 2005). "Supporting cast's vibrancy saves 'Face'". The Boston Globe. Retrieved 17 July 2009.
Jump up ^ Park, Ed (17 May 2005). "Film". Village Voice. p. 1. Retrieved 17 July 2009.
^ Jump up to: a b Rosenbaum, Jonathan (9 February 2007). "Saving Face". Chicago Reader. Retrieved 17 July 2009.
Jump up ^ "Now, An Updated Edition Of The 102 Best Lesbian Movies Of All Time". Autostraddle. 2017-02-14. Retrieved 2017-07-08.
Jump up ^ "Saving Face". Rotten Tomatoes. IGN. Retrieved 17 July 2009.
Jump up ^ "Saving Face". Metacritic. Retrieved 17 July 2009.
^ Jump up to: a b c d "Saving Face (2004)- Awards". IMDB. Retrieved 17 July 2009.
External links[edit]
Official website
Saving Face on IMDb
Saving Face at AllMovie
AfterEllen.com Interview with Michelle Krusiec and Lynn Chen
Saving Face at Rotten Tomatoes
Retrieved from "https://en.wikipedia.org/w/index.php?title=Saving_Face_(2004_film)&oldid=800687671"
Categories:
2004 films
2000s comedy-drama films
2000s romantic comedy films
American films
American romantic comedy films
American comedy-drama films
American LGBT-related films
Chinese-American films
Taiwanese-American films
LGBT-related comedy films
English-language films
Mandarin-language films
Shanghainese-language films
Lesbian-related films
Sony Pictures Classics films
Destination Films films
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