{"title":"Inhibitors of fibrinolysis in the treatment of haemophilia.","authors":"C R Rizza","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75996,"journal":{"name":"Journal of clinical pathology. Supplement (Royal College of Pathologists)","volume":"14 ","pages":"50-4"},"PeriodicalIF":0.0,"publicationDate":"1980-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1347106/pdf/jclinpath00431-0055.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18049316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Breakdown products of fibrin and fibrinogen: molecular mechanisms and clinical implications.","authors":"P J Gaffney","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75996,"journal":{"name":"Journal of clinical pathology. Supplement (Royal College of Pathologists)","volume":"14 ","pages":"10-7"},"PeriodicalIF":0.0,"publicationDate":"1980-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1347099/pdf/jclinpath00431-0015.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17506056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Natural inhibitors of fibrinolysis.","authors":"D Collen","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75996,"journal":{"name":"Journal of clinical pathology. Supplement (Royal College of Pathologists)","volume":"14 ","pages":"24-30"},"PeriodicalIF":0.0,"publicationDate":"1980-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1347101/pdf/jclinpath00431-0029.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17506059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Biological role of fibrinolysis.","authors":"J F Davidson, I D Walker","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75996,"journal":{"name":"Journal of clinical pathology. Supplement (Royal College of Pathologists)","volume":"14 ","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"1980-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1347097/pdf/jclinpath00431-0006.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17506053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Biochemistry of the plasmin system.","authors":"D Ogston","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75996,"journal":{"name":"Journal of clinical pathology. Supplement (Royal College of Pathologists)","volume":"14 ","pages":"5-9"},"PeriodicalIF":0.0,"publicationDate":"1980-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1347098/pdf/jclinpath00431-0010.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17506057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Antifibrinolytic therapy in genitourinary tract surgery.","authors":"L Andersson","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75996,"journal":{"name":"Journal of clinical pathology. Supplement (Royal College of Pathologists)","volume":"14 ","pages":"60-2"},"PeriodicalIF":0.0,"publicationDate":"1980-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1347108/pdf/jclinpath00431-0065.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17983494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Antibody function is a property of the immunoglobulins. Therefore antibody deficiency in its severest form implies immunoglobulin deficiency or agammaglobulinaemia. Since most patients with antibody deficiency produce at least some immunoglobulin, the term hypogammaglobulinaemia is to be preferred to the more absolute agammaglobulinae.mia. Hypogammaglobulinaemia due to a failure of antibody synthesis may be congenital or acquired, primary or secondary. This failure of synthesis is usually associated with a lack of mature plasma cells and rather less commonly with a lack of B lymphocytes. Immunoglobulin deficiency may affect all classes but often may be restricted to only one or two classes or subclasses. Rare individuals show a functional antibody deficiency despite quantitatively normal amounts of all immunoglobulin classes. The spectrum of primary antibody deficiency syndromes is shown in Table 1. Secondary antibody deficiency due to immunoglobulin loss usually affects mainly IgG and is associated with a degree of hypoproteinaemia and hypoalbuminaemia.
{"title":"Diagnosis of defects of antibody production.","authors":"A M Ward","doi":"10.1136/jcp.s3-13.1.23","DOIUrl":"https://doi.org/10.1136/jcp.s3-13.1.23","url":null,"abstract":"Antibody function is a property of the immunoglobulins. Therefore antibody deficiency in its severest form implies immunoglobulin deficiency or agammaglobulinaemia. Since most patients with antibody deficiency produce at least some immunoglobulin, the term hypogammaglobulinaemia is to be preferred to the more absolute agammaglobulinae.mia. Hypogammaglobulinaemia due to a failure of antibody synthesis may be congenital or acquired, primary or secondary. This failure of synthesis is usually associated with a lack of mature plasma cells and rather less commonly with a lack of B lymphocytes. Immunoglobulin deficiency may affect all classes but often may be restricted to only one or two classes or subclasses. Rare individuals show a functional antibody deficiency despite quantitatively normal amounts of all immunoglobulin classes. The spectrum of primary antibody deficiency syndromes is shown in Table 1. Secondary antibody deficiency due to immunoglobulin loss usually affects mainly IgG and is associated with a degree of hypoproteinaemia and hypoalbuminaemia.","PeriodicalId":75996,"journal":{"name":"Journal of clinical pathology. Supplement (Royal College of Pathologists)","volume":"13 ","pages":"23-5"},"PeriodicalIF":0.0,"publicationDate":"1979-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/jcp.s3-13.1.23","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"11598743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
About two-thirds of tumours of adult human lymphoid tissue originate from B cells; one-fifth derive from T cells; one-eighth are undefinable, using markers currently available; and fewer than one in a 100 are truely histiocytic, showing markers associated with monocytes (Lukes et al., 1978). B cells can be demonstrated in suitable tissue sections since they possess either surface or intracytoplasmic immunoglobulin. Evidence of monoclonality can be deduced from the pattern of immunoglobulin light chain staining (Warnke and Levy, 1978). Techniques are not yet available to enable similarly detailed studies to be performed on human T cells in tissue sections where structural relationships can be defined. The emphasis in this paper consequently is on B cell malignancies.
{"title":"Distribution of malignant lymphoid cells.","authors":"R I Vanhegan","doi":"10.1136/jcp.s3-13.1.70","DOIUrl":"https://doi.org/10.1136/jcp.s3-13.1.70","url":null,"abstract":"About two-thirds of tumours of adult human lymphoid tissue originate from B cells; one-fifth derive from T cells; one-eighth are undefinable, using markers currently available; and fewer than one in a 100 are truely histiocytic, showing markers associated with monocytes (Lukes et al., 1978). B cells can be demonstrated in suitable tissue sections since they possess either surface or intracytoplasmic immunoglobulin. Evidence of monoclonality can be deduced from the pattern of immunoglobulin light chain staining (Warnke and Levy, 1978). Techniques are not yet available to enable similarly detailed studies to be performed on human T cells in tissue sections where structural relationships can be defined. The emphasis in this paper consequently is on B cell malignancies.","PeriodicalId":75996,"journal":{"name":"Journal of clinical pathology. Supplement (Royal College of Pathologists)","volume":"13 ","pages":"70-5"},"PeriodicalIF":0.0,"publicationDate":"1979-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/jcp.s3-13.1.70","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"11598746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The formation of antibodies has been the subject of hypothesis and experimentation for the whole of this century. Our knowledge of antibody formation has made dramatic advances on several occasions. Many of these advances have become crystallised as certainties in the text books. The fascination of the subject, however, has always been its uncertainties, which have continued to undermine the text book picture of antibody formation. As ever in research, the questions are more important than the answers. For an understanding of antibody formation, or of any other biological system, one must ultimately turn to the molecular level. This necessity was plainly seen by Roy Cameron who, in recreating his research department in 1946, 'determined to explore the new techniques for examination of cell fractions, and lethal syntheses, and biochemical lesions in the cell' (Oakley, 1968). Progress in the study of antibody formation during the past three decades has been achieved by exploring the paths pointed out by Roy Cameron. Those paths have led us well over any horizon that could have been foreseen in 1946 and even beyond horizons visible in 1966. At our present stage in the exploration I will attempt to draw together the apparent certainties and indicate some of the uncertainties. I will begin with the beguiling question of antibody diversity, a subject for which the cellular, genetic, and molecular basis continues to hold many uncertainties.
{"title":"Roy Cameron lecture. Control of antibody formation: certain uncertainties.","authors":"A R Williamson","doi":"10.1136/jcp.s3-13.1.76","DOIUrl":"https://doi.org/10.1136/jcp.s3-13.1.76","url":null,"abstract":"The formation of antibodies has been the subject of hypothesis and experimentation for the whole of this century. Our knowledge of antibody formation has made dramatic advances on several occasions. Many of these advances have become crystallised as certainties in the text books. The fascination of the subject, however, has always been its uncertainties, which have continued to undermine the text book picture of antibody formation. As ever in research, the questions are more important than the answers. For an understanding of antibody formation, or of any other biological system, one must ultimately turn to the molecular level. This necessity was plainly seen by Roy Cameron who, in recreating his research department in 1946, 'determined to explore the new techniques for examination of cell fractions, and lethal syntheses, and biochemical lesions in the cell' (Oakley, 1968). Progress in the study of antibody formation during the past three decades has been achieved by exploring the paths pointed out by Roy Cameron. Those paths have led us well over any horizon that could have been foreseen in 1946 and even beyond horizons visible in 1966. At our present stage in the exploration I will attempt to draw together the apparent certainties and indicate some of the uncertainties. I will begin with the beguiling question of antibody diversity, a subject for which the cellular, genetic, and molecular basis continues to hold many uncertainties.","PeriodicalId":75996,"journal":{"name":"Journal of clinical pathology. Supplement (Royal College of Pathologists)","volume":"13 ","pages":"76-84"},"PeriodicalIF":0.0,"publicationDate":"1979-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/jcp.s3-13.1.76","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"11598747","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The aim of this short review is to describe the role of the major histocompatibility complex (MHC) in the regulation of T lymphocyte function.This genetic complex, which includes the immune response (Ir) genes, imposes certain restrictions on the immune system. The clinical relevance of these findings is indicated by the well-known associations between particular HLA antigens and disease susceptibility. An abnormal immune response appears to play a major role in the pathogenesis of many of these diseases.
{"title":"Lymphocytes. 1. Function. Genetic restrictions in the immune response.","authors":"A J McMichael","doi":"10.1136/jcp.s3-13.1.30","DOIUrl":"https://doi.org/10.1136/jcp.s3-13.1.30","url":null,"abstract":"The aim of this short review is to describe the role of the major histocompatibility complex (MHC) in the regulation of T lymphocyte function.This genetic complex, which includes the immune response (Ir) genes, imposes certain restrictions on the immune system. The clinical relevance of these findings is indicated by the well-known associations between particular HLA antigens and disease susceptibility. An abnormal immune response appears to play a major role in the pathogenesis of many of these diseases.","PeriodicalId":75996,"journal":{"name":"Journal of clinical pathology. Supplement (Royal College of Pathologists)","volume":"13 ","pages":"30-8"},"PeriodicalIF":0.0,"publicationDate":"1979-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/jcp.s3-13.1.30","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"11314357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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