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A Bootello

Publications and source records attributed to A Bootello.

At least 55 records · Page 3Linked to original sources
PubMed1981

HLA antigens in a sample of the Spanish population: common features among Spaniards, Basques, and Sardinians.

Frequencies of recently described HLA-A,-B (antigens or splits) and HLA-C and HLA-DR antigens are studied in a 450 normal Spaniards sample. The linkage disequilibria are also calculated. HLA-DR7 is more frequent than in any other population studied. Aw30-B18 and Aw33-B14 associations are common and specific Spanish, Basque, and Sardinian HLA features. A11-B17 association is found in our Spanish sample and also in Basques. HLA-Bw4,-Bw6 antigens are analyzed by family mating and segregation and also using unrelated individuals. It shows a good fit as a genetic system. HLA-B antigens are included either in Bw4 or Bw6 according to expectations from other Caucasoid population results. The possibility of a common and North African origin (Iberians) for Spaniards, Basques, and Sardinians is discussed on the basis of presently available HLA data.

Female↗
PubMed1981

Bf polymorphism and its relationship with HLA antigens in a sample of the Spanish Population: high BfF1 frequencies.

Bf allele frequencies were studied in a sample of the normal Spanish population and in family haplotypes. BfF1 shows a frequency higher than in other Caucasoid populations and closer to that found in Negroids. Basques show an even higher BfF1 frequency BfF1 is in strong linkage disequilibrium with B18. HLA-Bw44 is found to be the B12 split in linkage disequilibrium with BfF and Bw50-BfS1 association is confirmed. DR3--BfF1 are not in linkage disequilibrium in the normal Spanish population, in contrast to DR3--BfF1 in linkage found in a diabetic Spanish population. Results are discussed on the bases of the paleo-North African Iberian population origins and of the use of Bf to define B12 and Bw21 splits.

Alleles↗
PubMed1981

Familial C1q deficiency associated with renal and cutaneous disease.

A familial C1q deficiency of complement in three siblings has been established. The patients were two brothers and a sister (12, 11 and 9 years old) with clinical and pathological features of Rothmund-Thomson syndrome (Poikiloderma congenital) and mesangial proliferative glomerulonephritis with diffuse IgM deposits. Abnormality has been defined as a total lack of CH50 haemolytic activity, undetectable C1q, failure to correct the defect with functionally pure C2 to C9 complement components, normal values for C2, C3, C4 and C5 and restoration of CH50 haemolytic activity when purified human C1q was added to the assay.

Adult↗
PubMed1978

Hepatocyte damage induced by lymphocytes from patients with chronic liver diseases, as detected by LDH release.

We have used a cytoplasmic enzyme system in the study of the in vitro cytotoxic activity of human peripheral blood leucocytes against isolated liver cells in patients with chronic liver diseases. Lymphocytes from primary biliary cirrhosis and chronic active liver disease patients were shown to have an in vitro capacity to induce a cytolitic effect on isolated hepatocytes, as demonstrated by the enhanced release of lactate dehydrogenase (LDH), a cytoplasmic marker enzyme. No significant LDH release was seen with control lymphocytes of normal persons or with lymphocytes from patients with alcoholic cirrhosis. Our results corroborate, in a different assay system, by a simple, reproducible and different method, that lymphocyte-mediated liver cell damage "in vitro" occurs in both primary biliary cirrhosis and chronic active liver disease.

Animals↗
PubMed1977

Immunological findings in immunoblastic lymphadenopathy. A detailed case study.

Several immunological parameters were investigated in a patient with immunoblastic lymphadenopathy (IBL). An increased concentration of polyclonal immunoglobulins, the presence of autoantibodies in the serum and an increased level of B lymphocytes with an abnormal DNA synthesis response to LPS in peripheral blood were the most salient features. The findings suggest that in IBL there is a numerical as well as a functional alteration of peripheral blood lymphocytes. We propose that the alteration was due to either an escape of lymphocytes from central lymphatic organs or a defect in maturation of peripheral blood lymphocytes.

Autoantibodies↗
PubMed1976

Injurious effect on rat liver mitochondria by lymphocytes from patients with primary biliary cirrhosis.

Lymphocytes from primary biliary cirrhosis (PBC) patients were shown to have an injurious effect on rat liver mitochondria, as was demonstrated by the inhibition of mitochondrial respiratory control by these cells. The incubation of the PBC patients' lymphocytes with isolated rat liver mitochondria produced a significant inhibition of mitochondrial respiration in the presence of ADP. However, no significant effect on respiration was seen with control lymphocytes of normal persons or with lymphocytes from patients with alcoholic cirrhosis and miscellaneous liver diseases. The results suggest that this injurious effect of PBC lymphocytes on mitochondria might be a consequence of sensitization in vivo of the PBC patients' lymphocytes by the mitochondrial antigens.

Animals↗
PubMed1975

Impairment of mitochondrial respiratory control by activated lymphocytes.

Mitochondria isolated from rat livers were used as a source of antigens capable of producing in vitro activation of lymphocytes that had previously been sensitized in vivo with the same antigen. Such lymphocytes were shown to have an injurious effect on target mitochondria, as was demonstrated by a new biochemical approach based on the study of the inhibition by these cells of mitochondrial respiratory control. A somewhat milder injurious capacity was also observed in normal and sensitized lymphocytes activated in vitro with the mitogen PHA. The lateration of the respiratory control of mitochondria by lymphocytes correlated with an increase in DNA synthesis in these cells.

Adenosine Diphosphate↗