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God bless you ma, it helped alot for my first professional today Thank you so much

Nice

Great video ❤

Wonderful 😊

Thanks

Thank you so much Ma'am, you are an amazing woman. ❤❤❤

This is a lifesaver. Revision couldn't have been made any easier. Thank you very much ma😊

Thank you for a wonderful lecture ma. can I get your lecture slides?

Thank you Ma for these expository lectures.

Serum contain L type monomer and here its given h type correct me plz.??

Thank you for the lecture Dr. Ify. From the lecture, am exposed to the knowledge of blood group which plays important role in lives of anaemic patients, transfusion and others. *Blood group is an inherence of the offspring from their parents. * The presence of antibiotics and antigen in the or on the surface of the RBC play key role in the classification of the human blood group. * There are more that 20 types of blood groups discovered. Such as ABO, P, Rhesus, KIDD, DIEGO. * Karl Landstainer discovered the ABO his coworkers discovered the Rhesus positive and negative (presence or absence). * He received noble award in 1930. * There are about 8 types of this blood group (ABO/rh) Such as A, B, AB, and 0. * A group contains A antigen and B antibodies. * B. Contains B antigen and A antibodies. * AB contains AB antigen but no antibodies * 0 contains no antigen on the RBC surface but A and B antibodies on the plasma. * The ABO gen is located in chromosome 9. * The neonate ABO can be detected at 6weeks before birth. * Blood group antigen are actually sugar attached to the RBC. * H gen cod the enzyme that add sugar fucose to the terminal sugar of the precursor substance. * Mixed cross match of this blood group leads to clinical complications, clumping, swallow of tissues, even death

Thank you ma for the Dr. Ify. From the lecture, am exposed to the knowledge of blood group which plays important role in lives of anaemic patients, transfusion and others. *Blood group is an inherence of the offspring from their parents. * The presence of antibiotics and antigen in the or on the surface of the RBC play key role in the classification of the human blood group. * There are more that 20 types of blood groups discovered. Such as ABO, P, Rhesus, KIDD, DIEGO. * Karl Landstainer discovered the ABO his coworkers discovered the Rhesus positive and negative (presence or absence). * He received noble award in 1930. * There are about 8 types of this blood group (ABO/rh) Such as A, B, AB, and 0. * A group contains A antigen and B antibodies. * B. Contains B antigen and A antibodies. * AB contains AB antigen but no antibodies * 0 contains no antigen on the RBC surface but A and B antibodies on the plasma. * The ABO gen is located in chromosome 9. * The neonate ABO can be detected at 6weeks before birth. * Blood group antigen are actually sugar attached to the RBC. * H gen cod the enzyme that add sugar fucose to the terminal sugar of the precursor substance. * Mixed cross match of this blood group leads to clinical complications, clumping, swallow of tissues, even death

In summary, I learnt about the brief history of the MNS blood group system. I learnt about the antigens in MNS blood group system which is about 43 in number but the prominent ones are the M,N,S and s antigens. However, this antigens of the MNS blood group system are carried on sugar bearing proteins called glycophorins which lies in the RBC membrane. The antibodies in this blood group system which are the IgM and IgG. The Ig class depends upon which antigen is targeted, also antibodies implicated in transfusion reaction. I learnt about the two genes that encode the MNS blood group which are; GYPA and GYPB, they are located at the long arm of chromosome 4 in the region of 4q28.2-q13.1. They are tightly linked and recombination occurs between them. I also learnt about the clinical importance of MNS antibodies which include; transfusion reaction and it also causes hemolytic disease of the new born. Thank you.

I Sincerely like to express my warmly greetings to you ma'am, Dr Ify, for taking time to explain vividly on the following: 1. Rh blood group system 2. The antigens in Rh blood group system. 3. Rh system antibody reactivity and characteristics 4. The genetics and inheritance of Rh antibodies 5. Lastly, clinical importance of Rh antibodies. Indeed you have done justice to the outlined above. From what I got. First of all, I learned that, Rh blood group is one of the most complex blood group known in human. The system is the 2nd most blood group system after ABO, especially in transfusion therapy and blood banking. The RHD antigen is highly immunogenic, which implies that it can trigger the production of anti-D antibodies in individuals who are RHD-negative . Moreso, I was able to understand the various Rh antigens which are approximately 50, with D, C, E, c and e as the most essential. They play an important role in determining an individual Rh status, which is either Rh-positive or RHD-negative, which varies on the presence or absence of the D antigen. Furthermore, the lecture expatiate, Rh antibodies are primarily of the IgG type and hardly activate the complement system. Instead, these antibodies bind to red blood cells, marking them for destruction in the spleen through a process known as extravascular hemolysis. It can lead severe hemolytic transfusion reaction. Interestingly, I learned much about genetics and inheritance of the Rh system. The Rh factor is inherited in a mendelian fashion, with Rh-positive being. Again, the clinical significance of the Rh factor especially in situations such as hemolytic disease of the newborn (HDN), where an RHD-negative mother carrying an Rh-positive fetus can develop anti-D antibodies. It can lead to complications in pregnancies if not properly managed. Finally, I learned the Rh system's significance in transfusion medicine, its genetic implications and the potential clinical challenges associated with Rh incompatibility. Progressively, you cleared my confusion about the, Kell blood system. From the lecture, the Kell blood system is a polymorphic system that carries complex enzymes that are highly immunogenic. In 1946, the Kell blood system was discovered by Mrs Keller whose antibodies led to haemolytic anemia of her stillborn child. Most importantly, you explained comprehensively about, ANTIGEN OF THE KELL BLOOD GROUP SYSTEM. There are 35 known antigens present in Kell blood group system, with ISBT Number -006. Also the two commonly encountered antigens are K and k. Meanwhile, the big K antigen is the most clinically significant Kell antigen. >>>The Kell protein is a polypeptide chain consisting of 732 amino acids that becomes glycosylated at five different sites. >>>The Kell glycoprotein is a transmembrane, single -pass protein that carries the Kell antigens. >>>Above All, I also understand the sequence of amino acids determine the specificity of the Kell antigen. My summary remains incomplete if I fail to appreciate your explanation about the, COMMON KELL PHENOTYPE. I learnt that; >>>The Kell blood system is complex . >>>The Kell locus is highly polymorphic and gives rise to many Kell antigens. >>>There are, however two major codominant allelic genes that produce two important antigens K and k (previously known as Kell and cellano, respectively), which differs by a single amino acid. THE UNCOMMON KELL PHENOTYPES. _NULL PHENOTYPE_ The Kell system has a rare null phenotype, K in which RBCs lack all Kell antigens. Individuals with this phenotype are healthy but produce anti-Ku when they encounter RBCs that do express Kell antigens. The explanation has been very interesting indeed Thanks very much Dr, for explaining detailed about the above topics. I have watched the video to the end and can assure you I understand every topic explained. Thanks once again.

Thank you very much madam for this video This video helped me to know about the history of the antigens, antibodies, and molecular basis of the globoside blood group system I learnt that the first antigen known as GLOB1 antigen was first discovered by Levine and Landsteeine in 1927 PI, Ike and Pk system were removed from the p system because they belong to Glob series glyco lipid, while Pi antigen is part of Neolactoseries. I also took note of the nature of antibodies and their reactivity. Thank you so much madam for this great lecture

Thank you, Dr. Maryann for this lecture. I got to understand the P1PK blood group system, from the history, discovery of P1P2 and also the new phenotype, PK that was later discovered and another antigen NOR which was also discovered as a part of the P1PK blood group. Also the discovery of the gene A4GALT which encodes as 4-alpha-galactosyltansferase enzyme that catalyses the reaction that synthesises P1 and PK antigens. I understand that individuals with P1 phenotype have more active enzyme than individuals with P2 phenotype. And also in a sense that different alleles of the gene A4GALT determine the P1, Pk and NOR antigens which P1 alleles encodes both P1 and P antigens while P2 encode only PK and rare NOR alleles encodes P1 and P. anti-P1, anti-P, anti-PK, antiP1PPK and anti-NOR antibodies are reactivated to P1Pk phenotypes

Thank you ma for this wonderful lectures on Kidd blood group system. I learnt that Kidd system was named after a patient. Here is my summary on this , the Kidd blood group system discovered in 1951 and composed of two antithetical antigens jka along with a third high-incident antigens jks The nature of the Kidd antigens are proteins and they are limited to RBc and kidney. The have functions, genetics , frequencies , phenotype and their functions

Thank you ma for this wonderful lectures on Kidd blood group system. I learnt that Kidd system was named after a patient. Here is my summary on this , the Kidd blood group system discovered in 1951 and composed of two antithetical antigens jka along with a third high-incident antigens jks The nature of the Kidd antigens are proteins and they are limited to RBc and kidney. The have functions, genetics , frequencies , phenotype and their functions

Thank you ma for this wonderful lectures on Kidd blood group system. I learnt that Kidd system was named after a patient. Here is my summary on this , the Kidd blood group system discovered in 1951 and composed of two antithetical antigens jka along with a third high-incident antigens jks The nature of the Kidd antigens are proteins and they are limited to RBc and kidney. The have functions, genetics , frequencies , phenotype and their functions

Thank you ma for this wonderful lectures on Kidd blood group system. I learnt that Kidd system was named after a patient. Here is my summary on this , the Kidd blood group system discovered in 1951 and composed of two antithetical antigens jka along with a third high-incident antigens jks The nature of the Kidd antigens are proteins and they are limited to RBc and kidney. The have functions, genetics , frequencies , phenotype and their functions

Thank you ma for this wonderful lecture on Kidd blood group system. I learnt that it is named after a woman Mrs. Kidd in whom the first antibody was isolated in 1951, during her pregnancy. The antigen of Kidd blood group system are jka, jkb and jk3 antigens. The first example of null phenotype [jk(a-b)] was discovered in 1959. The antigens of Kidd blood group are proteins and are limited to red blood cells (RBCs) membrane and the kidney( in the vasa recta). The Kidd protein is a major transporter of urea in RBCS and also maintain osmotic stability. But deficiencies of this Kidd protein lead to no severe health conditions. The solute carrier family 14, member 1 ( SLC14A1) gene encodes the Kidd glycoprotein and it is located on chromosome 18 and 11 exons of which only exons 4-11 encode the mature Kidd protein. Jka and jkb are the two major codominant alleles of SLC14A1 and they differ by a single amino acid. The jk(a-b-) phenotype is inherited as a recessive trait. It has been found that the percentage/ frequency of Kidd antigen found in various population are ; Jka: 77%cucasians, 92%blacks and 73%Asians Jkb:74%cucasians , 43% black and 76% Asians Jk3:100% in most population and 99% in Polynesians. Aside jk(a-b-) other phenotype are jk( a+b),jk(a-b+),jk(a+b+). The null phenotype jk (a-b-) is rare in most population and after immunization, it forms anti- jk3.

Thank you Dr. for this wonderful session. During the lesson I learnt that the Duffy blood Group system was discovered in 1950 by cutbish, Mollison and Parkin and named after the patient (Mr. Duffy) whom it was discovered. it was also identified in haemophiliac patient after multiple transfusion. The Duffy blood Group system has an ISBT symbol of FY and ISBT No 008, with six known blood Group antigen (Fya, Fyb, Fy3, Fy4, Fy5 and Fy6). The Duffy antigen is a glycoprotein with a transmembrane with RBC, N-terminal domain, and cytoplasmisc C terminal domain. This antigen are found on RBC, endothelial cells, epithelial cells of the kidney collection duct, thyroid glands, and colon, and spleen, and surface of purkinje cells etc. The Duffy glycoprotein function in inflammatory processes (chemo kine receptors), it serves as a receptor for plasmodium knowlensi and P. Vivax that invade the RBC. Also they are immune antibodies mainly the IgG. ANTIBODY REACTIVITY: Fya and Fyb antigens are destroyed by peoteolytic enzymes eg papain therefore do not react by enzyme technique also the storage of RBC in low PH and less solution causes progression loss of antigen reactivity. THE DUFFY PHENOTYPE: Consist of four main phenotypes these are: 1. FY (a+b-) have duffy A antigen but no Duffy B antigen 2. FY (a+b+) have both Duffy A and B antigens 3. FY (a-b+) no Duffy A antigen but have Duffy B antigen. 4 FY (a-b-) do no have Duffy A and B antigens (Duffy null phenotype-the Duffy null phenotype is the most common antigen in black people. They are negative phenotype but can expressed the phenotype on other part of the body. this could arise as a result of mutation in the promoter region of the Fyb allele. THE DUFFY ANTIGEN AND MALARIA PARASITE RELATIONSHIP. Plasmodium falciparium specie routinely causes malaria but in Asians and America, P. Vivax is the most common cause of disease by binding to the Duffy N terminal extracellular domain of the glycoprotein thro the cystein region of the Duffy binding protein, however individuals with the null phenotype do not expressed Duffy protein on the RBC as such they are immune to P. vivax. THE CLINIAL SIGNIFICANCE OF DUFFY ANTIBODIES 1. Transfusion reaction 2 mild hemolytic disease of the new born. Thank you Ma.

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Thank you ma for the wonderful lecture Here is my summary: The Duffy blood group was identified in 1950 by Cutbush, Mollison, and Parkin. Later, they discovered an antibody known as anti-Fy² in the serum of a patient with hemophilia who had received multiple transfusions. This antibody was named after the patient, Mr. Duffy. The Duffy blood group system consists of the following antigens: Fya, Fyb, Fy3, Fy4, Fy5, and Fy6. These antigens are found in various locations, including red blood cells, collecting ducts, endothelial cells lining blood vessels, lung alveoli, and on the surface of Purkinje cells in the cerebellum. The genetics of Duffy antigens are controlled by the FY gene, with FYA and FYB as the primary alleles. These antigens follow Mendelian inheritance patterns, and their frequency varies among different populations. There is a significant relationship between Duffy antigens and malaria. The parasite Plasmodium vivax, a major cause of malaria, must bind to the N-terminal extracellular domain of Duffy glycoproteins on red blood cells to enter and infect them. Individuals with the Duffy null phenotype, who do not express Duffy proteins on their red blood cells, are resistant to P. vivax infection. Clinically, Duffy antibodies are important because they can: i. Cause hemolytic disease in newborns. ii. Serve as binding sites for Plasmodium vivax, certain chemokines, and the parasite Plasmodium knowlesi. iii. Be responsible for adverse reactions during blood transfusions.

Thank you ma for this lecture series. I learnt that the MNS blood group system was discovered in 1927 after the discovery of ABO blood group system in 1900 The MNS has 43 antigens including M,N,S and s antigens.The s antigens doffers by a change in 1 amino acid. S is more commonly seen in M(+) than M(-). M and N phenotype differs from each other by 1 amino acid of position I and S in the extracellular N-terminal domain. There are inherited in an autosomal codominant pattern, located on chromosome 4q28--q32. There is the presence of M,N,S and S antigens determined by GYPB gene expression. Clinical important of blood group system are; .Antibodies can cause HDN .Transfusion reactions . Haemolytic disease of the newborn (HDN). Thank you once again ma David ita Faculty of medical laboratory science University of calabar

Thank u ma

Thanks alot Mum 🎉

Very educative

Thank you very much for the lecture ma. I learnt that Blood grouping classifies blood based on antigens on red blood cells (RBCs). Human RBCs have various surface antigens and immune properties. There are over 20 blood groups, but ABO and Rhesus (Rh) are most important. Karl Landsteiner discovered the ABO system in 1901, identifying the A, B, and O groups. The AB group was later discovered by his students in 1902. The ABO blood groups are A, B, AB, and O. The ABO gene is on chromosome 9, with A and B being dominant over O. Landsteiner’s rule states: if an antigen is on a red blood cell, the corresponding antibody will not be in the plasma.

I'm expressing my heartfelt gratitude for your clear and concise lecture on MNS blood group systems. Your teaching style and enthusiasm made the complex topic easy to understand and engaging. Your lecture summary helped me grasp the key points, including: - The MNS blood group system is a classification of human blood based on the presence or absence of specific antigens on red blood cells - The three main antigens in the MNS system are M, N, and S - The possible genotypes and phenotypes of the MNS blood group system - The importance of understanding blood group systems in transfusion medicine Your dedication to teaching and your ability to break down complex concepts into simple, understandable language are truly appreciated. Thank you for helping me understand the MNS blood group system and its significance in the medical field.

Thank you very much ma’m for this wonderful lectures, in summary, i learnt that there is a blood group named (Diego blood group). It was discovered in the year 1955, and it was name after a lady Diego. Diego blood group system are complex blood group system that have several antigens on the surface of the RBC. And is associated with the gene known as SLC4A1 ( it is also known as anion exchanger).it encodes a substance called band 3 protein, which is expressed on the surface of the red blood cells and plays a Central role in mediating the transport of carbon dioxide in the blood. And there are 22 diego blood group known presently with three of high prevelalance and some being antithetical to each other which are Dia, Dib, and Wra. Antigens of the diego blood group are carriers of important protein called BAND 3 protein which lies in the RBC membrane and is found in the kidney where it is involved in acid secretion. This band 3 protein is an important integral protein of the BC membrane. And its clinical importance, they are commonly associated with HDFN, and they are more common in south east Asia and South America. And hemolytic disease in new Born.

Thank you ma for this brain feeding lecture . SUMMARY OF THE MNS BLOOD GROUP SYSTEM. • It was the second blood group that was discovered by Landsteiner and his colleagues in 1927 after the discovery of the first blood group system which is the "ABO" in 1900. In their experiment, they immunized rabbit with human blood cell. During the process some antigen M and antigen N, antigen S and antigen s were named. Antigen MN and Ss alleles are gene linked on chromosome 4 which belong to single bond blood group system. "The number of the antigens blood group system are 43 but the prominent ones are M,N,S and s • The ISBT symbol is given as MNS °ISBT number is 02. "Antigens are proteins. "Amino acid sequence determines the specificity of MNS antigens *The antigens of the MNS blood group are carried on sugar bearing proteins called Glycophorins. These lies in the red blood cell(RBC) membrane • one end of a Glycophorin is attached to theunderlying cell, and the other end bears the sugar and determines a person's MNS blood type. *The MNS antigens differ by 2 amino acid. • Glycoprotein antigens are destroyed by enzyme treatment. They have dosage effects/quantitative variants °S/s antigen differ by a change in 1 amino acid. S is more commonly seen in M+ than M-. Because they have dosage effect they are needed in homozygous form. The molecules that carry the MNS antigens are Glycophorin A and B. The MNS antigens are found mainly on RBCs(Red blood cells). There are about 1 million copies of Glycophorin A per RBC and 0.2million copies of Glycophorin B. The MNS antigens are also expressed in the kidney on the renal endothelium and epithelium. • The frequency of MNS antigens (%); M: 78% Caucasians, 74% Blacks, N:72% Caucasians, 75% Blacks S:55% caucasians, 31% Blacks s: 89% Caucasians, 93% Blacks.The latter two phenotypes are common in Blacks also. Occuring at a frequency of 33% and 19% respectively. For the antibodies to MNS antigens, they are the IgG and IgM. The Ig class depends upon which antigen is targeted. Anti S and anti s are generally immune and rarely produced. The two genes encoded in the Glycophorins that carry the antigens of the MNS blood group are the GYPA and GYPB. clinical importance of MNS antibodies include: *Transfusion reaction * Haemolytic disease of the newborn.

Thank you so much for this lecture, ma'am. I gained valuable insights from the video and now have a much clearer understanding of blood group systems, particularly the Rhesus (Rh) factor. The Rh system is the second most critical blood group system after ABO, especially in transfusion therapy and blood banking. The RHD antigen is highly immunogenic, meaning it can trigger the production of anti-D antibodies in individuals who are RHD-negative. The lecture covered the various Rh antigens, noting that there are approximately 50, with D, C, E, c, and e being the most significant. These antigens play a crucial role in determining an individual's Rh status, which is either Rh-positive or Rh-negative, depending on the presence or absence of the D antigen. I also learned that Rh antibodies are primarily of the IgG type and rarely activate the complement system. Instead, these antibodies bind to red blood cells, marking them for destruction in the spleen through a process known as extravascular hemolysis. This can lead to severe hemolytic transfusion reactions, especially when antibodies such as anti-D, anti-C, anti-E, and anti-c are involved. The lecture also delved into the genetics and inheritance of Rh antigens. The Rh factor is inherited in a Mendelian fashion, with Rh-positive being dominant over Rh-negative. For instance, if one parent is Rh-positive (either DD or Dd) and the other is Rh-negative (dd), their child could be either Rh-positive or Rh-negative. Even if both parents are Rh-positive, if one carries the recessive Rh-negative allele (Dd), there is still a possibility of having an Rh-negative child. In addition, I learned about the clinical significance of the Rh factor, especially in scenarios such as hemolytic disease of the newborn (HDN), where an Rh-negative mother carrying an Rh-positive fetus can develop anti-D antibodies. This can lead to serious complications in subsequent pregnancies if not properly managed. Overall, the lecture provided me with a comprehensive understanding of the Rh system's importance in transfusion medicine, its genetic implications, and the potential clinical challenges associated with Rh incompatibility.

In summary The Duffy blood group was discovered by Cutbush,Mollison and Parkin in 1950 They later discovered what was known as anti-Fy² in the serum of a multi transfused haemophiliac patient and was later named after the patient Mr. Duffy in whom the antibody was found. The antigens in Duffy blood group system system are as follows: Fya, Fyb, Fy3 ,Fy4, Fy5 and Fy6. They are located in the Red blood Cells (RBC), Collecting ducts, endothelial cells that line the blood vessels,lung alveovi and the surface of Purkinje cells of the cerebellum in the brain. The genetics of Duffy antigens is that it is encoded by the FY gene which has FYA and FYB as by the main alleles They are in inherited in a Mendelian fashion Also the frequency of Duffy entities tend to vary among populations. The relationship between Duffy antigens and malaria parasite infection is that Plasmodium valvax is a major cause of Malaria and to cause the disease; plasmodium valvax must enter the red blood cells by binding to the N- terminal extracellular domain of the Duffy glycoproteins through the cysteine -rich region of the Duffy binding protein. People with Duffy null phenotype do not express the Duffy protein on their red blood cells are immune to P. vilvax infection Clinical importance of Duffy antibodies are: 1. They cause haemolytic diseases in infants 2. They also act as binding sites for plasmodium valvax,chemokins and knowlesi 3.They are also responsible for blood transfusion reaction. Thank you for the lecture Looking forward to more.

"Thank you for the insightful lecture on the Kell blood group system! I gained a deeper understanding of this complex system, which contains multiple highly immunogenic antigens. These antigens vary in frequency across populations and are third in triggering immune responses, after ABO and Rh systems. The Kell system, discovered in 1946, is named after Mrs. Kelleher, whose antibodies caused hemolytic disease in her child. It comprises 35 recognized antigens, with K and k being the most significant. The Kell protein, a 732-amino-acid polypeptide, is glycosylated and anchored to RBC surfaces via XK protein. Its absence leads to McLeod's syndrome. The KEL gene, located on chromosome 7, exhibits high polymorphism with codominant alleles k and K. Kell antigens are found on erythroid and myeloid cells, functioning as endothelin-3-converting enzymes. Immune Kell antibodies (mainly IgG) can cause severe hemolytic reactions. Key points: - Highly polymorphic Kell locus - Rare null phenotype (ko) requires ko-compatible blood products - K antigen is highly immunogenic - Anti-Kell causes HDN, especially in mothers with prior transfusions - Inherited antigen system, with parental antigens determining offspring expression Your lecture skillfully clarified the intricacies of the Kell blood group system.

This is interesting ma, i have learnt that: H blood group wasa discovered in bombay, india, in an individual with interesting blood type that reacted to other blood types in an unknown way. It has only one antigen, the H antigen which is indirectly encoded by FUT1 and FUT2 genes. The H antigen was discovered in 1952 by doctor YM bhende. It shares the same blood tissue distribution as A and B antigens and it is found in all fluids except cerebrospinal fluid. H phenotypes present are secretor (common) and non secretor (common). In secretor: H antigen is expressed on RBCs and saliva. In non secretor: H antigen is absent in saliva bit present on RBCs. In both phenotypes: There is no anti H produced. It has H/H or H/h; Se/Se genotype. The frequency of H antigen is 99.9% on the red blood cells. Anti H reactivity shows that it is capable of hemolysis. It may also be involved in cell adhesion. Thanks for this ma, much appreciated.

Your lecture Gracie's me, Thanks Ma ,I learnt that the globoside consist of two main antigen p and p1. The p antigen is present on red blood cells of most individual while the p1 , antigen is present on red blood cells of approximately 79percent of individuals .

Greeting ma, thanks for the enlightenment. Here are some things I've learnt from this lecture MNS blood group. MNS was the second blood group discovered in 1927 after the discovery of the blood groups ABO, in 1900. Number of MNS antigen are: 43 including M,N,S and s ISBT symbol: MNS ISBT number: 02 MNS antigen Amino acid sequence determine the specificery of MNS antigen. These be in the red blood cell (RBC). Genetic and inheritance The MNS blood group was inherited in an autosomal pattern. It's located at the chromosome. Clinical importance are Haemolytic disease of the newborn. Transfusion reactions Thank you ma for your Time.

Greeting ma, thanks for the enlightenment. Here are some things I've learnt from this lecture MNS blood group. MNS was the second blood group discovered in 1927 after the discovery of the blood groups ABO, in 1900. Number of MNS antigen are: 43 including M,N,S and s ISBT symbol: MNS ISBT number: 02 MNS antigen Amino acid sequence determine the specificery of MNS antigen. These be in the red blood cell (RBC). Genetic and inheritance The MNS blood group was inherited in an autosomal pattern. It's located at the chromosome. Clinical importance are Haemolytic disease of the newborn. Transfusion reactions Thank you ma for your Time.

Thank u very much ma for this wonderful lecture, This lecturer has brought me to understand that P1pk blood group system was formally known as P blood system, discovered by Landsteiner and Levine in the year 1927, it happened that they found a new antigen present on the erythrocytes of about 80% of individuals and where termed P ( +) and absent in others that where termed ( P_) individuals which means it was defined by an antibody ( anti P) and antigen ( antigen P) The number of antigens 3 ( p1kp and Nor) gene symbol A4GALT ( alpha _4 Nacetyl galactic saminytransferase) cod ( course of defferentiation): CD77, chromosomal Location 22a 13.2 P1 is very much active enzyme that produces both p1 and Pk antigens but the p2 is a less active enzyme that only produces PK . P1 and Pk antigens in the A4GALT synthesis show that the P1PK are carbohydrates P1 antigen carbohydrates occurs on glycolipids and glycoprotein while pk only knows as aglobo series glycoid. The P1 phenotype has both P1 and Pk antigens while the P2 phenotype has just one pk antigen, The cause of this is because the variation of the enzyme produced s by the AGALT gene. THANK YOU MA.

"Thank you for the enlightening lecture on the Kell blood group system! I gained valuable insights into this intricate complex. In essence, the Kell blood group system comprises multiple highly immunogenic antigens, ranking third in triggering immune responses after ABO and Rh systems. These antigens exhibit varying frequencies across populations. Discovered in 1946, the Kell system honors Mrs. Kelleher, whose antibodies caused hemolytic disease in her child. It encompasses 35 recognized antigens (ISBT 006) and features two prominent antigens, K and k. The K antigen holds significant clinical importance. The Kell protein, a 732-amino-acid polypeptide, undergoes glycosylation at five sites. Its specificity is determined by amino acid sequences, and it's anchored to RBC surfaces via an integral protein, XK. The absence of XK leads to McLeod's syndrome. Located on chromosome 7 (7q33), the KEL gene spans 19 exons and 21 kbp, exhibiting high polymorphism with codominant alleles k and K, differing by a single amino acid and nucleotide. Kell antigens appear on erythroid and myeloid cells, functioning as endothelin-3-converting enzymes. Immune Kell antibodies (mainly IgG) can cause severe hemolytic reactions. Antigens K and anti-K typically exhibit IgG immune responses, activating complement and reacting optimally at 37°C via AGH and enzyme techniques. However, some anti-K reactions may be weaker in LISS. Both antigens can provoke hemolytic transfusion reactions and hemolytic disease of the newborn (HDN), potentially severe or fatal. Key points: - Highly polymorphic Kell locus - Rare null phenotype (ko) requires ko-compatible blood products - K antigen is highly immunogenic - Anti-Kell causes HDN, particularly in mothers with prior transfusions - Inherited antigen system, where parental antigens determine offspring expression Your lecture expertly unraveled the complexities of the Kell blood group system!" Thank u so much ma 😊

I was able to understand that H blood group was first discovered in bombay India and that it reacts with other rbcs from ABO group like O cells, A cell ,B cell, Ab cell It possess one antigen and that's the H antigen. I was also made to understand that they share broad tissue that can be found on the surface of red cell and other cell and also tissue, the H blood group the chromosome is located on the 19 at 13.3 The group locus and the secretors locus contain the FUT1 and FUT2 gene And I was made to understand that FUT1 encodes indirectly for the expression of H antigen on the surface of the cell and this is possible through fucosyltransferase while FUT2 encodes a double form of H antigen that is find in the blood fluid of secretors Bombastic phenotype is the absence of H antigen and fucose is the terminal sugar needed in the formation of H antigen The clinical significance is the transfusion reaction and hemolytic disease of new born.

Thanks dr ify on your intensive lecture. The Duffy blood group system's complexities have significant implications for transfusion safety and malaria research. I'm struck by the potential for Duffy antigen research to inform targeted therapies for Plasmodium vivax and P. knowlesi infections. The clarification on anti-Fy3's role in delayed transfusion reactions underscores the importance of meticulous antibody screening in transfusion medicine. Furthermore, the intricate binding sites in the extracellular domain offer a fascinating area for further exploration. I'm excited to investigate how this knowledge can be leveraged to develop novel diagnostics and therapeutics, ultimately enhancing patient outcomes in transfusion medicine and malaria-endemic regions.

In summary I was ableist to understand that the H blood group system is not a separate blood group like ABO or MNS, but rather a precursor to the ABO system. The H antigen is present on the surface of red blood cells and serves as the foundation for the A and B antigens. The H antigen is necessary for the production of A and B antigens, so individuals with a H blood group deficiency may have an O blood type. Also, the clinical implication of being a Bombay group O individual, is that the patient can only receive blood transfusions from a Bombay donor, due to the presence of powerful anti- H antibodies in their serum, only blood products belonging to the same blood group can be administered to them. And incompatible blood transfusion leads to hemolytic transfusion reaction.

Dr ify Thank you for the insightful lecture on the Duffy blood group system! I gained a deeper understanding of the complex interactions between Duffy antigens and antibodies. The revelation that RBCs lacking Duffy antigens are resistant to Plasmodium vivax and P. knowlesi infections has significant implications for malaria research. I also appreciate the clarification on anti-Fy3's role in delayed transfusion reactions. The overview of the six known antigens (FYa, FYb, FY, FY*, and Fy) and their overlapping binding sites in the extracellular domain has solidified my grasp of this intricate system. Your explanation has sparked my interest in further exploring the clinical applications of this knowledge.

Dr ify Thank you for the insightful lecture on the Duffy blood group system! I gained a deeper understanding of the complex interactions between Duffy antigens and antibodies. The revelation that RBCs lacking Duffy antigens are resistant to Plasmodium vivax and P. knowlesi infections has significant implications for malaria research. I also appreciate the clarification on anti-Fy3's role in delayed transfusion reactions. The overview of the six known antigens (FYa, FYb, FY, FY*, and Fy) and their overlapping binding sites in the extracellular domain has solidified my grasp of this intricate system. Your explanation has sparked my interest in further exploring the clinical applications of this knowledge.

Dr ify Thank you for the insightful lecture on the Duffy blood group system! I gained a deeper understanding of the complex interactions between Duffy antigens and antibodies. The revelation that RBCs lacking Duffy antigens are resistant to Plasmodium vivax and P. knowlesi infections has significant implications for malaria research. I also appreciate the clarification on anti-Fy3's role in delayed transfusion reactions. The overview of the six known antigens (FYa, FYb, FY, FY*, and Fy) and their overlapping binding sites in the extracellular domain has solidified my grasp of this intricate system. Your explanation has sparked my interest in further exploring the clinical applications of this knowledge.

Dr ify Thank you for the insightful lecture on the Duffy blood group system! I gained a deeper understanding of the complex interactions between Duffy antigens and antibodies. The revelation that RBCs lacking Duffy antigens are resistant to Plasmodium vivax and P. knowlesi infections has significant implications for malaria research. I also appreciate the clarification on anti-Fy3's role in delayed transfusion reactions. The overview of the six known antigens (FYa, FYb, FY, FY*, and Fy) and their overlapping binding sites in the extracellular domain has solidified my grasp of this intricate system. Your explanation has sparked my interest in further exploring the clinical applications of this knowledge.

Thank you so much for this video ma, I learnt that Duffy blood group was discovered in 1950 by a group of scientist namely cutbush, mollisol and parkin. There are two types of Duffy blood group,Duffy positive and Duffy negative.The video explained the different entities within the system,the antibodies associated with it and how this antibodies are inherited. There are six known entities :Fya,Fyb,Fy3,Fy4,Fy5 and Fy6.the antigens acts as receptors for chemokines and malaria parasites. Individuals lacking Duffy antigens are resistant to certain malaria parasites. Overall, this video helped me understand the importance of the Duffy blood group system in blood transfusions and the prevention of certain diseases

Thank you ma for this educative session. I Learnt that the kidd system was named after a patient,Mrs Kidd in 1951 during her pregnancy. It is named after the protein on the surface of Red Blood Cell called KIDD ANTIGENS which contains 3 antigen JK1(JKa), JK2(JKb) and JK3.The JKa was the first antigen to be discovered and two others antigens JKb and JK3.The Anti JK3 can cause severe and fatal hemolytic transfusion commonly associated with less severe DHTRs In kidd antigens,Antibodies were produced/belonged to 1gG and 1gM Immunoglobulin causing hemolysis. The genetic of Kidd blood system is the SLC14A1 gene which conceal the kiddo glycoprotein. The phenotype ranges from JK(a-b+) to JK(a+b+) with Jk(a-b-) Individuals. The practical Significance or Clinical Importance of kidd antibodies are often difficult to detect,making them hazardous in transfusion medicine,where they are suspected to be a common cause of Delayed Haemolytic Transfusion Reactions.